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    <title>Sinapsos Podcast | Oncology</title>
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    <description><![CDATA[<p><strong>Zero Fluff. Pure Insight.</strong></p>
<p>Get the latest scientific research without the small talk. We dive deep into new publications to give you clear, information-packed summaries—no filler, no chatter.</p>
<p><b>Stay tuned. Stay informed.</b></p>]]></description>
    <pubDate>Fri, 30 Oct 2026 11:09:19 +0000</pubDate>
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        <copyright>Copyright 2025 All rights reserved.</copyright>
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    <item>
        <title>E47 - Liquid Biopsy for Lung Cancer Care</title>
        <itunes:title>E47 - Liquid Biopsy for Lung Cancer Care</itunes:title>
        <link>https://sinapsospodcast-oncology.podbean.com/e/e47-liquid-biopsy-for-lung-cancer-care/</link>
                    <comments>https://sinapsospodcast-oncology.podbean.com/e/e47-liquid-biopsy-for-lung-cancer-care/#comments</comments>        <pubDate>Fri, 30 Oct 2026 11:09:19 +0000</pubDate>
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                                    <description><![CDATA[<p>E47   |  9 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/19/3140'>Publication Link</a>
</p>
<ul>
    <li>Podcast based on: Mansour, H.; Mazouji, O.; El Hammouti, A.; Alloubi, I.; Incitti, R.; El Kazzouli, S.; Ouhajjou, A.; Nejjari, C. Refining Lung Cancer Care: The Emerging Role of Liquid Biopsy in Screening, Diagnosis, and Precision Oncology. Cancers 2026, 18, 3140. https://doi.org/10.3390/cancers18193140
Type: Review  |  Publication date: 28 September 2026

</li>
    <li>Summary: Researchers reviewed the emerging role of liquid biopsy in lung cancer care. Using a narrative review and a structured search of the ClinicalTrials.gov registry, they examined clinically endorsed uses of liquid biopsy for guiding treatment in advanced lung cancer and investigational uses for early detection, while also considering challenges of current technologies, artificial intelligence, and implementation. Current evidence supports liquid biopsy for molecular profiling and treatment selection in advanced non-small cell lung cancer. Its use in early detection, screening, and minimal residual disease-guided management remains investigational and requires further prospective validation. Because low-dose computed tomography screening has limitations such as false-positive findings and restricted accessibility, liquid biopsy is seen as a promising non-invasive complementary approach to tissue biopsy and screening technology and, in some cases, an alternative. It may help advance precision oncology and improve lung cancer management.

</li>
    <li>Keywords: lung cancer; blood test; screening; diagnosis; follow up; treatment guidance; non-invasive; genetic test; epigenetic test; liquid biopsy</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E47   |  9 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/19/3140'>Publication Link</a><br>
</p>
<ul>
    <li>Podcast based on: Mansour, H.; Mazouji, O.; El Hammouti, A.; Alloubi, I.; Incitti, R.; El Kazzouli, S.; Ouhajjou, A.; Nejjari, C. Refining Lung Cancer Care: The Emerging Role of Liquid Biopsy in Screening, Diagnosis, and Precision Oncology. Cancers 2026, 18, 3140. https://doi.org/10.3390/cancers18193140<br>
Type: Review  |  Publication date: 28 September 2026<br>
<br>
</li>
    <li>Summary: Researchers reviewed the emerging role of liquid biopsy in lung cancer care. Using a narrative review and a structured search of the ClinicalTrials.gov registry, they examined clinically endorsed uses of liquid biopsy for guiding treatment in advanced lung cancer and investigational uses for early detection, while also considering challenges of current technologies, artificial intelligence, and implementation. Current evidence supports liquid biopsy for molecular profiling and treatment selection in advanced non-small cell lung cancer. Its use in early detection, screening, and minimal residual disease-guided management remains investigational and requires further prospective validation. Because low-dose computed tomography screening has limitations such as false-positive findings and restricted accessibility, liquid biopsy is seen as a promising non-invasive complementary approach to tissue biopsy and screening technology and, in some cases, an alternative. It may help advance precision oncology and improve lung cancer management.<br>
<br>
</li>
    <li>Keywords: lung cancer; blood test; screening; diagnosis; follow up; treatment guidance; non-invasive; genetic test; epigenetic test; liquid biopsy</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
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        <itunes:summary><![CDATA[E47   |  9 min   |   Latest   |  Publication Link

    Podcast based on: Mansour, H.; Mazouji, O.; El Hammouti, A.; Alloubi, I.; Incitti, R.; El Kazzouli, S.; Ouhajjou, A.; Nejjari, C. Refining Lung Cancer Care: The Emerging Role of Liquid Biopsy in Screening, Diagnosis, and Precision Oncology. Cancers 2026, 18, 3140. https://doi.org/10.3390/cancers18193140Type: Review  |  Publication date: 28 September 2026
    Summary: Researchers reviewed the emerging role of liquid biopsy in lung cancer care. Using a narrative review and a structured search of the ClinicalTrials.gov registry, they examined clinically endorsed uses of liquid biopsy for guiding treatment in advanced lung cancer and investigational uses for early detection, while also considering challenges of current technologies, artificial intelligence, and implementation. Current evidence supports liquid biopsy for molecular profiling and treatment selection in advanced non-small cell lung cancer. Its use in early detection, screening, and minimal residual disease-guided management remains investigational and requires further prospective validation. Because low-dose computed tomography screening has limitations such as false-positive findings and restricted accessibility, liquid biopsy is seen as a promising non-invasive complementary approach to tissue biopsy and screening technology and, in some cases, an alternative. It may help advance precision oncology and improve lung cancer management.
    Keywords: lung cancer; blood test; screening; diagnosis; follow up; treatment guidance; non-invasive; genetic test; epigenetic test; liquid biopsy

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>522</itunes:duration>
                        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E46 - Nodal Staging in Locally Advanced Lung Cancer</title>
        <itunes:title>E46 - Nodal Staging in Locally Advanced Lung Cancer</itunes:title>
        <link>https://sinapsospodcast-oncology.podbean.com/e/e53-nodal-staging-in-locally-advanced-lung-cancer/</link>
                    <comments>https://sinapsospodcast-oncology.podbean.com/e/e53-nodal-staging-in-locally-advanced-lung-cancer/#comments</comments>        <pubDate>Mon, 21 Sep 2026 07:30:33 +0100</pubDate>
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                                    <description><![CDATA[<p>E46   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/16/2561'>Publication Link</a>
</p>
<ul>
    <li>Podcast based on: Haimi, I.; Rajaram, R. Nodal Staging in Patients with Locally Advanced Non-Small Cell Lung Cancer: Indications, Approaches, and Impact on Downstream Treatment Selection. Cancers 2026, 18, 2561. https://doi.org/10.3390/cancers18162561
Type: Review  |  Publication date: 10 August 2026

</li>
    <li>Summary: Precise mediastinal lymph node staging is fundamental to the management of locally advanced non-small cell lung cancer (NSCLC). Nodal disease status is the primary determinant of prognosis in this population and directly governs eligibility for surgery, multimodality therapy, immunotherapy, and molecularly targeted treatments. As systemic options expand and therapeutic sequencing becomes increasingly complex, accurate nodal assessment is more critical than ever. This review examines contemporary mediastinal staging approaches and illustrates how nodal evaluation drives modern treatment selection in stage II-III NSCLC.

</li>
    <li>Keywords: non-small cell lung cancer; mediastinal lymph node staging; endobronchial ultrasound-guided transbronchial needle aspiration; FDG-PET/CT; neoadjuvant chemoimmunotherapy; N2 disease classification; TNM ninth edition; perioperative immunotherapy; surgical resection; multidisciplinary treatment planning</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E46   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/16/2561'>Publication Link</a><br>
</p>
<ul>
    <li>Podcast based on: Haimi, I.; Rajaram, R. Nodal Staging in Patients with Locally Advanced Non-Small Cell Lung Cancer: Indications, Approaches, and Impact on Downstream Treatment Selection. Cancers 2026, 18, 2561. https://doi.org/10.3390/cancers18162561<br>
Type: Review  |  Publication date: 10 August 2026<br>
<br>
</li>
    <li>Summary: Precise mediastinal lymph node staging is fundamental to the management of locally advanced non-small cell lung cancer (NSCLC). Nodal disease status is the primary determinant of prognosis in this population and directly governs eligibility for surgery, multimodality therapy, immunotherapy, and molecularly targeted treatments. As systemic options expand and therapeutic sequencing becomes increasingly complex, accurate nodal assessment is more critical than ever. This review examines contemporary mediastinal staging approaches and illustrates how nodal evaluation drives modern treatment selection in stage II-III NSCLC.<br>
<br>
</li>
    <li>Keywords: non-small cell lung cancer; mediastinal lymph node staging; endobronchial ultrasound-guided transbronchial needle aspiration; FDG-PET/CT; neoadjuvant chemoimmunotherapy; N2 disease classification; TNM ninth edition; perioperative immunotherapy; surgical resection; multidisciplinary treatment planning</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
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        <itunes:summary><![CDATA[E46   |  11 min   |   Latest   |  Publication Link

    Podcast based on: Haimi, I.; Rajaram, R. Nodal Staging in Patients with Locally Advanced Non-Small Cell Lung Cancer: Indications, Approaches, and Impact on Downstream Treatment Selection. Cancers 2026, 18, 2561. https://doi.org/10.3390/cancers18162561Type: Review  |  Publication date: 10 August 2026
    Summary: Precise mediastinal lymph node staging is fundamental to the management of locally advanced non-small cell lung cancer (NSCLC). Nodal disease status is the primary determinant of prognosis in this population and directly governs eligibility for surgery, multimodality therapy, immunotherapy, and molecularly targeted treatments. As systemic options expand and therapeutic sequencing becomes increasingly complex, accurate nodal assessment is more critical than ever. This review examines contemporary mediastinal staging approaches and illustrates how nodal evaluation drives modern treatment selection in stage II-III NSCLC.
    Keywords: non-small cell lung cancer; mediastinal lymph node staging; endobronchial ultrasound-guided transbronchial needle aspiration; FDG-PET/CT; neoadjuvant chemoimmunotherapy; N2 disease classification; TNM ninth edition; perioperative immunotherapy; surgical resection; multidisciplinary treatment planning

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>608</itunes:duration>
                <itunes:episode>49</itunes:episode>
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    <item>
        <title>E45 - Antibody-Drug Conjugates in Contemporary Oncology</title>
        <itunes:title>E45 - Antibody-Drug Conjugates in Contemporary Oncology</itunes:title>
        <link>https://podcast.sinapsos.com/e/e45-antibody-drug-conjugates-in-contemporary-oncology/</link>
                    <comments>https://podcast.sinapsos.com/e/e45-antibody-drug-conjugates-in-contemporary-oncology/#comments</comments>        <pubDate>Wed, 16 Sep 2026 16:21:07 +0100</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/6157dd3a-6503-505e-940b-380e818bc670</guid>
                                    <description><![CDATA[<p>E45   |  19 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/16/2652'>Publication Link</a>
</p>
<ul>
    <li>Podcast based on: Philipovskiy, A.; Shurmur, S.; Abid, M.B. Antibody–Drug Conjugates in Contemporary Oncology: A Clinical Perspective on Dose Optimization, Sequencing, and Combination Strategies. Cancers 2026, 18, 2652. https://doi.org/10.3390/cancers18162652
Type: Review  |  Publication date: 17 August 2026

</li>
    <li>Summary: Antibody–drug conjugates are cancer treatments designed to deliver potent cytotoxic drugs more selectively to tumor cells by linking a tumor-directed antibody to a therapeutic payload. This review examines the structural and biologic features that determine clinical activity, including target selection, linker stability, payload class, drug-to-antibody ratio, tumor penetration, biomarkers, toxicity, and resistance. Particular attention is given to the practical questions emerging as multiple ADCs enter the same malignancies and earlier treatment settings: how to select a biologically efficient dose, how to sequence agents with overlapping targets or payloads, and how to distinguish rational combinations from combinations that merely add toxicity. The next phase of ADC development will require not only improved molecular engineering, but also a more disciplined clinical framework for selecting, dosing, sequencing, and combining these agents.

</li>
    <li>Keywords: antibody–drug conjugates; dose optimization; sequencing; combination strategies; biomarkers; resistance; interstitial lung disease; linker; payload; translational oncology</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E45   |  19 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/16/2652'>Publication Link</a><br>
</p>
<ul>
    <li>Podcast based on: Philipovskiy, A.; Shurmur, S.; Abid, M.B. Antibody–Drug Conjugates in Contemporary Oncology: A Clinical Perspective on Dose Optimization, Sequencing, and Combination Strategies. Cancers 2026, 18, 2652. https://doi.org/10.3390/cancers18162652<br>
Type: Review  |  Publication date: 17 August 2026<br>
<br>
</li>
    <li>Summary: Antibody–drug conjugates are cancer treatments designed to deliver potent cytotoxic drugs more selectively to tumor cells by linking a tumor-directed antibody to a therapeutic payload. This review examines the structural and biologic features that determine clinical activity, including target selection, linker stability, payload class, drug-to-antibody ratio, tumor penetration, biomarkers, toxicity, and resistance. Particular attention is given to the practical questions emerging as multiple ADCs enter the same malignancies and earlier treatment settings: how to select a biologically efficient dose, how to sequence agents with overlapping targets or payloads, and how to distinguish rational combinations from combinations that merely add toxicity. The next phase of ADC development will require not only improved molecular engineering, but also a more disciplined clinical framework for selecting, dosing, sequencing, and combining these agents.<br>
<br>
</li>
    <li>Keywords: antibody–drug conjugates; dose optimization; sequencing; combination strategies; biomarkers; resistance; interstitial lung disease; linker; payload; translational oncology</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
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        <itunes:summary><![CDATA[E45   |  19 min   |   Latest   |  Publication Link

    Podcast based on: Philipovskiy, A.; Shurmur, S.; Abid, M.B. Antibody–Drug Conjugates in Contemporary Oncology: A Clinical Perspective on Dose Optimization, Sequencing, and Combination Strategies. Cancers 2026, 18, 2652. https://doi.org/10.3390/cancers18162652Type: Review  |  Publication date: 17 August 2026
    Summary: Antibody–drug conjugates are cancer treatments designed to deliver potent cytotoxic drugs more selectively to tumor cells by linking a tumor-directed antibody to a therapeutic payload. This review examines the structural and biologic features that determine clinical activity, including target selection, linker stability, payload class, drug-to-antibody ratio, tumor penetration, biomarkers, toxicity, and resistance. Particular attention is given to the practical questions emerging as multiple ADCs enter the same malignancies and earlier treatment settings: how to select a biologically efficient dose, how to sequence agents with overlapping targets or payloads, and how to distinguish rational combinations from combinations that merely add toxicity. The next phase of ADC development will require not only improved molecular engineering, but also a more disciplined clinical framework for selecting, dosing, sequencing, and combining these agents.
    Keywords: antibody–drug conjugates; dose optimization; sequencing; combination strategies; biomarkers; resistance; interstitial lung disease; linker; payload; translational oncology

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1080</itunes:duration>
                <itunes:episode>47</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E44 - Exercise Program for Cancer Fatigue</title>
        <itunes:title>E44 - Exercise Program for Cancer Fatigue</itunes:title>
        <link>https://podcast.sinapsos.com/e/e44-exercise-program-for-cancer-fatigue/</link>
                    <comments>https://podcast.sinapsos.com/e/e44-exercise-program-for-cancer-fatigue/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:23:18 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/b2432477-9e39-3343-ba99-e639751c24cd</guid>
                                    <description><![CDATA[<p>E44   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/947'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Cano-Uceda, A.; Pareja-García, P.; Sánchez-Rodríguez, E.; Fraguas-Ramos, D.; Martín-Álvarez, L.; Asencio-Vicente, R.; Rivero-de la Villa, A.; Pérez-Pérez, M.d.M.; Obispo-Portero, B.M.; Morales-Ruiz, L.; de Dios-Álvarez, R.; Sanchez-Barroso, L.; De Sousa-De Sousa, L.; Maté-Muñoz, J.L.; García-Fernández, P. Effects of a 6-Week Supervised Multimodal Exercise Program on Cancer-Related Fatigue, Quality of Life and Physical Function During Active Treatment: A Randomized Controlled Trial. Cancers 2026, 18, 947. https://doi.org/10.3390/cancers18060947
Type: Article  |  Publication date: 13 March 2026

</li>
<li>Summary: Reduced quality of life, cancer-related fatigue, and functional impairment are common problems during and after cancer treatment. To examine this issue, a randomized clinical trial was conducted with 110 patients with stage I–III cancer. Participants were randomly assigned either to an intervention group, which completed a six-week supervised exercise program, or to a control group that received usual care. The exercise program included cardiorespiratory training, strength exercises, and stretching, with intensity monitored through perceived exertion. Quality of life, fatigue, functional capacity, and muscle strength were assessed. The group that completed the exercise program showed significant and clinically meaningful improvements in fatigue, global quality of life, functional capacity, and muscle strength compared with the control group. Furthermore, a higher percentage of participants in the intervention group achieved improvements considered clinically important. Among symptoms, only insomnia showed a significant reduction. Conclusion: A brief, supervised therapeutic exercise program of moderate to vigorous intensity is safe and effective for improving fatigue, quality of life, and physical function in patients with cancer, and may be suitable for integration into routine oncologic care.

</li>
<li>Keywords: therapeutic exercise; cancer; quality of life; physical function; fatigue; short-duration intervention</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E44   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/947'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Cano-Uceda, A.; Pareja-García, P.; Sánchez-Rodríguez, E.; Fraguas-Ramos, D.; Martín-Álvarez, L.; Asencio-Vicente, R.; Rivero-de la Villa, A.; Pérez-Pérez, M.d.M.; Obispo-Portero, B.M.; Morales-Ruiz, L.; de Dios-Álvarez, R.; Sanchez-Barroso, L.; De Sousa-De Sousa, L.; Maté-Muñoz, J.L.; García-Fernández, P. Effects of a 6-Week Supervised Multimodal Exercise Program on Cancer-Related Fatigue, Quality of Life and Physical Function During Active Treatment: A Randomized Controlled Trial. Cancers 2026, 18, 947. https://doi.org/10.3390/cancers18060947<br>
Type: Article  |  Publication date: 13 March 2026<br>
<br>
</li>
<li>Summary: Reduced quality of life, cancer-related fatigue, and functional impairment are common problems during and after cancer treatment. To examine this issue, a randomized clinical trial was conducted with 110 patients with stage I–III cancer. Participants were randomly assigned either to an intervention group, which completed a six-week supervised exercise program, or to a control group that received usual care. The exercise program included cardiorespiratory training, strength exercises, and stretching, with intensity monitored through perceived exertion. Quality of life, fatigue, functional capacity, and muscle strength were assessed. The group that completed the exercise program showed significant and clinically meaningful improvements in fatigue, global quality of life, functional capacity, and muscle strength compared with the control group. Furthermore, a higher percentage of participants in the intervention group achieved improvements considered clinically important. Among symptoms, only insomnia showed a significant reduction. Conclusion: A brief, supervised therapeutic exercise program of moderate to vigorous intensity is safe and effective for improving fatigue, quality of life, and physical function in patients with cancer, and may be suitable for integration into routine oncologic care.<br>
<br>
</li>
<li>Keywords: therapeutic exercise; cancer; quality of life; physical function; fatigue; short-duration intervention</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/v68z35nesqfvwqj9/E44_-_Exercise_Program_for_Cancer_Fatigue.mp3" length="25809858" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E44   |  18 min   |   Latest   |  Publication Link

Podcast based on: Cano-Uceda, A.; Pareja-García, P.; Sánchez-Rodríguez, E.; Fraguas-Ramos, D.; Martín-Álvarez, L.; Asencio-Vicente, R.; Rivero-de la Villa, A.; Pérez-Pérez, M.d.M.; Obispo-Portero, B.M.; Morales-Ruiz, L.; de Dios-Álvarez, R.; Sanchez-Barroso, L.; De Sousa-De Sousa, L.; Maté-Muñoz, J.L.; García-Fernández, P. Effects of a 6-Week Supervised Multimodal Exercise Program on Cancer-Related Fatigue, Quality of Life and Physical Function During Active Treatment: A Randomized Controlled Trial. Cancers 2026, 18, 947. https://doi.org/10.3390/cancers18060947Type: Article  |  Publication date: 13 March 2026
Summary: Reduced quality of life, cancer-related fatigue, and functional impairment are common problems during and after cancer treatment. To examine this issue, a randomized clinical trial was conducted with 110 patients with stage I–III cancer. Participants were randomly assigned either to an intervention group, which completed a six-week supervised exercise program, or to a control group that received usual care. The exercise program included cardiorespiratory training, strength exercises, and stretching, with intensity monitored through perceived exertion. Quality of life, fatigue, functional capacity, and muscle strength were assessed. The group that completed the exercise program showed significant and clinically meaningful improvements in fatigue, global quality of life, functional capacity, and muscle strength compared with the control group. Furthermore, a higher percentage of participants in the intervention group achieved improvements considered clinically important. Among symptoms, only insomnia showed a significant reduction. Conclusion: A brief, supervised therapeutic exercise program of moderate to vigorous intensity is safe and effective for improving fatigue, quality of life, and physical function in patients with cancer, and may be suitable for integration into routine oncologic care.
Keywords: therapeutic exercise; cancer; quality of life; physical function; fatigue; short-duration intervention

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1075</itunes:duration>
                <itunes:episode>45</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E43 - Endometrial Cancer Prognosis Study</title>
        <itunes:title>E43 - Endometrial Cancer Prognosis Study</itunes:title>
        <link>https://podcast.sinapsos.com/e/e43-endometrial-cancer-prognosis-study/</link>
                    <comments>https://podcast.sinapsos.com/e/e43-endometrial-cancer-prognosis-study/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:22:18 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/fbc5c010-9693-3f2f-9485-26767d7acd99</guid>
                                    <description><![CDATA[<p>E43   |  15 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/929'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Paratore, S.; Russo, A.; Lanzafame, K.; Blanco, G.; Giurato, E.; Bartoloni, G.; D’Asta, M.; Sapienza, M.; Bonanno, G.M.; Vallone, A.; Ettore, G.; Bordonaro, R. Prognostic Stratification of Multiple-Classifier Endometrial Cancers: Cohort Study and Meta-Analysis. Cancers 2026, 18, 929. https://doi.org/10.3390/cancers18060929
Type: Article  |  Publication date: 12 March 2026

</li>
<li>Summary: The classification of endometrial cancer has evolved using molecular features, allowing for improved risk assessment and more personalized treatment strategies. However, a small proportion of tumors show more than one relevant molecular alteration, making their classification and clinical management more challenging. This study aimed to characterize molecular and clinicopathological profiles of multiple-classifier endometrial cancers, enhancing our understanding of their biological heterogeneity. In our patient cohort, POLEmut tumors with concurrent MMRd/MSI generally retained the POLE-associated ultramutated profile, while tumors with both MMRd/MSI and p53abn/TP53mut alterations were more often associated with more adverse clinicopathological characteristics compared to MMRd/MSI-only tumors. By integrating our data in a systematic literature review with meta-analysis, we observed that variability in reported incidence is largely driven by differences in testing strategies. These results highlight the limitations of current classification systems and emphasize the importance of more standardized molecular approaches to improve risk stratification and management in endometrial cancer.

</li>
<li>Keywords: endometrial cancer; molecular profile; clinicopathological features; multiple-classifier; POLE mutated; mismatch repair-deficient; TP53mutated; next generation sequencing</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E43   |  15 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/929'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Paratore, S.; Russo, A.; Lanzafame, K.; Blanco, G.; Giurato, E.; Bartoloni, G.; D’Asta, M.; Sapienza, M.; Bonanno, G.M.; Vallone, A.; Ettore, G.; Bordonaro, R. Prognostic Stratification of Multiple-Classifier Endometrial Cancers: Cohort Study and Meta-Analysis. Cancers 2026, 18, 929. https://doi.org/10.3390/cancers18060929<br>
Type: Article  |  Publication date: 12 March 2026<br>
<br>
</li>
<li>Summary: The classification of endometrial cancer has evolved using molecular features, allowing for improved risk assessment and more personalized treatment strategies. However, a small proportion of tumors show more than one relevant molecular alteration, making their classification and clinical management more challenging. This study aimed to characterize molecular and clinicopathological profiles of multiple-classifier endometrial cancers, enhancing our understanding of their biological heterogeneity. In our patient cohort, POLEmut tumors with concurrent MMRd/MSI generally retained the POLE-associated ultramutated profile, while tumors with both MMRd/MSI and p53abn/TP53mut alterations were more often associated with more adverse clinicopathological characteristics compared to MMRd/MSI-only tumors. By integrating our data in a systematic literature review with meta-analysis, we observed that variability in reported incidence is largely driven by differences in testing strategies. These results highlight the limitations of current classification systems and emphasize the importance of more standardized molecular approaches to improve risk stratification and management in endometrial cancer.<br>
<br>
</li>
<li>Keywords: endometrial cancer; molecular profile; clinicopathological features; multiple-classifier; POLE mutated; mismatch repair-deficient; TP53mutated; next generation sequencing</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/2sr767efcajreyg2/E43_-_Endometrial_Cancer_Prognosis_Study.mp3" length="21245744" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E43   |  15 min   |   Latest   |  Publication Link

Podcast based on: Paratore, S.; Russo, A.; Lanzafame, K.; Blanco, G.; Giurato, E.; Bartoloni, G.; D’Asta, M.; Sapienza, M.; Bonanno, G.M.; Vallone, A.; Ettore, G.; Bordonaro, R. Prognostic Stratification of Multiple-Classifier Endometrial Cancers: Cohort Study and Meta-Analysis. Cancers 2026, 18, 929. https://doi.org/10.3390/cancers18060929Type: Article  |  Publication date: 12 March 2026
Summary: The classification of endometrial cancer has evolved using molecular features, allowing for improved risk assessment and more personalized treatment strategies. However, a small proportion of tumors show more than one relevant molecular alteration, making their classification and clinical management more challenging. This study aimed to characterize molecular and clinicopathological profiles of multiple-classifier endometrial cancers, enhancing our understanding of their biological heterogeneity. In our patient cohort, POLEmut tumors with concurrent MMRd/MSI generally retained the POLE-associated ultramutated profile, while tumors with both MMRd/MSI and p53abn/TP53mut alterations were more often associated with more adverse clinicopathological characteristics compared to MMRd/MSI-only tumors. By integrating our data in a systematic literature review with meta-analysis, we observed that variability in reported incidence is largely driven by differences in testing strategies. These results highlight the limitations of current classification systems and emphasize the importance of more standardized molecular approaches to improve risk stratification and management in endometrial cancer.
Keywords: endometrial cancer; molecular profile; clinicopathological features; multiple-classifier; POLE mutated; mismatch repair-deficient; TP53mutated; next generation sequencing

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>885</itunes:duration>
                <itunes:episode>44</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E42 - Brain Tumor Review Molecular Diversity</title>
        <itunes:title>E42 - Brain Tumor Review Molecular Diversity</itunes:title>
        <link>https://podcast.sinapsos.com/e/e42-brain-tumor-review-molecular-diversity/</link>
                    <comments>https://podcast.sinapsos.com/e/e42-brain-tumor-review-molecular-diversity/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:21:17 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/0a1a280b-2efb-3f1c-ac1a-bc1078f08efd</guid>
                                    <description><![CDATA[<p>E42   |  20 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/912'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Lee, C.; Park, K.; Park, S.; Kim, M.; Hwang, J. Diffuse Leptomeningeal Glioneuronal Tumor: A Systematic Review Highlighting Molecular Heterogeneity and Survival Outcome. Cancers 2026, 18, 912. https://doi.org/10.3390/cancers18060912
Type: Systematic Review  |  Publication date: 11 March 2026

</li>
<li>Summary: Diffuse leptomeningeal glioneuronal tumor is a very rare brain tumor that mainly affects children and young adults and often spreads along the brain and spinal cord. Because it is uncommon and difficult to diagnose, treatment strategies vary widely and clinical outcomes remain unpredictable. To address this, we reviewed all published cases reported since this tumor was first defined to summarize clinical features, genetic findings, treatments, and survival outcomes. We found that hydrocephalus and spinal involvement were common, and that surgery was associated with longer survival in selected patients. Genetic alterations affecting tumor growth–related pathways were also frequently observed. This summary of current evidence may help clinicians recognize this tumor earlier and consider appropriate management strategies.

</li>
<li>Keywords: diffuse leptomeningeal glioneuronal tumor; leptomeningeal dissemination; BRAF fusion; MAPK pathway; pediatric low-grade glioma; molecular heterogeneity; survival analysis</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E42   |  20 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/912'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Lee, C.; Park, K.; Park, S.; Kim, M.; Hwang, J. Diffuse Leptomeningeal Glioneuronal Tumor: A Systematic Review Highlighting Molecular Heterogeneity and Survival Outcome. Cancers 2026, 18, 912. https://doi.org/10.3390/cancers18060912<br>
Type: Systematic Review  |  Publication date: 11 March 2026<br>
<br>
</li>
<li>Summary: Diffuse leptomeningeal glioneuronal tumor is a very rare brain tumor that mainly affects children and young adults and often spreads along the brain and spinal cord. Because it is uncommon and difficult to diagnose, treatment strategies vary widely and clinical outcomes remain unpredictable. To address this, we reviewed all published cases reported since this tumor was first defined to summarize clinical features, genetic findings, treatments, and survival outcomes. We found that hydrocephalus and spinal involvement were common, and that surgery was associated with longer survival in selected patients. Genetic alterations affecting tumor growth–related pathways were also frequently observed. This summary of current evidence may help clinicians recognize this tumor earlier and consider appropriate management strategies.<br>
<br>
</li>
<li>Keywords: diffuse leptomeningeal glioneuronal tumor; leptomeningeal dissemination; BRAF fusion; MAPK pathway; pediatric low-grade glioma; molecular heterogeneity; survival analysis</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/pu2jiivncaftx9rf/E42_-_Brain_Tumor_Review_Molecular_Diversity.mp3" length="27416075" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E42   |  20 min   |   Latest   |  Publication Link

Podcast based on: Lee, C.; Park, K.; Park, S.; Kim, M.; Hwang, J. Diffuse Leptomeningeal Glioneuronal Tumor: A Systematic Review Highlighting Molecular Heterogeneity and Survival Outcome. Cancers 2026, 18, 912. https://doi.org/10.3390/cancers18060912Type: Systematic Review  |  Publication date: 11 March 2026
Summary: Diffuse leptomeningeal glioneuronal tumor is a very rare brain tumor that mainly affects children and young adults and often spreads along the brain and spinal cord. Because it is uncommon and difficult to diagnose, treatment strategies vary widely and clinical outcomes remain unpredictable. To address this, we reviewed all published cases reported since this tumor was first defined to summarize clinical features, genetic findings, treatments, and survival outcomes. We found that hydrocephalus and spinal involvement were common, and that surgery was associated with longer survival in selected patients. Genetic alterations affecting tumor growth–related pathways were also frequently observed. This summary of current evidence may help clinicians recognize this tumor earlier and consider appropriate management strategies.
Keywords: diffuse leptomeningeal glioneuronal tumor; leptomeningeal dissemination; BRAF fusion; MAPK pathway; pediatric low-grade glioma; molecular heterogeneity; survival analysis

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1142</itunes:duration>
                <itunes:episode>43</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E41 - Lipid Changes in Leukemia Diagnosis</title>
        <itunes:title>E41 - Lipid Changes in Leukemia Diagnosis</itunes:title>
        <link>https://podcast.sinapsos.com/e/e41-lipid-changes-in-leukemia-diagnosis/</link>
                    <comments>https://podcast.sinapsos.com/e/e41-lipid-changes-in-leukemia-diagnosis/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:20:16 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/1c8b61f9-de68-3b2e-a857-2769a4908476</guid>
                                    <description><![CDATA[<p>E41   |  22 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/896'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Wojnicka, J.; Kiełbus, M.; Mertowska, P.; Mertowski, S.; Grywalska, E.; Sosnowski, P.; Wielgosz, A.; Kozub-Pędrak, A.; Sosnowska-Pasiarska, B.; Klatka, M.; Klatka, J.; Błażewicz, A. Specific Lipidomic Shifts in Chronic Lymphocytic Leukemia at Diagnosis. Cancers 2026, 18, 896. https://doi.org/10.3390/cancers18060896
Type: Article  |  Publication date: 10 March 2026

</li>
<li>Summary: Chronic lymphocytic leukemia (CLL) is a common type of adult blood cancer in which cells survive longer than normal, partly due to changes in how they process fats and other molecules for energy. This study examined the blood plasma of newly diagnosed patients who had not yet received treatment to identify unique patterns in lipid molecules. We found that patients with CLL had higher levels of certain fats, including carnitines and specific phospholipids, compared with healthy individuals. By analyzing these lipid changes using predictive bioinformatics tools, we identified that several pathways involved in lipid metabolism are likely disrupted. These findings improve our understanding of how this disease alters the body’s metabolism and could inform future research on biomarkers for earlier disease detection and treatment development.

</li>
<li>Keywords: chronic lymphocytic leukemia (CLL); metabolic reprogramming; carnitines; ether-linked phospholipids; lipidomics</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E41   |  22 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/6/896'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Wojnicka, J.; Kiełbus, M.; Mertowska, P.; Mertowski, S.; Grywalska, E.; Sosnowski, P.; Wielgosz, A.; Kozub-Pędrak, A.; Sosnowska-Pasiarska, B.; Klatka, M.; Klatka, J.; Błażewicz, A. Specific Lipidomic Shifts in Chronic Lymphocytic Leukemia at Diagnosis. Cancers 2026, 18, 896. https://doi.org/10.3390/cancers18060896<br>
Type: Article  |  Publication date: 10 March 2026<br>
<br>
</li>
<li>Summary: Chronic lymphocytic leukemia (CLL) is a common type of adult blood cancer in which cells survive longer than normal, partly due to changes in how they process fats and other molecules for energy. This study examined the blood plasma of newly diagnosed patients who had not yet received treatment to identify unique patterns in lipid molecules. We found that patients with CLL had higher levels of certain fats, including carnitines and specific phospholipids, compared with healthy individuals. By analyzing these lipid changes using predictive bioinformatics tools, we identified that several pathways involved in lipid metabolism are likely disrupted. These findings improve our understanding of how this disease alters the body’s metabolism and could inform future research on biomarkers for earlier disease detection and treatment development.<br>
<br>
</li>
<li>Keywords: chronic lymphocytic leukemia (CLL); metabolic reprogramming; carnitines; ether-linked phospholipids; lipidomics</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/m96h4c2e368isuhz/E41_-_Lipid_Changes_in_Leukemia_Diagnosis.mp3" length="30286828" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E41   |  22 min   |   Latest   |  Publication Link

Podcast based on: Wojnicka, J.; Kiełbus, M.; Mertowska, P.; Mertowski, S.; Grywalska, E.; Sosnowski, P.; Wielgosz, A.; Kozub-Pędrak, A.; Sosnowska-Pasiarska, B.; Klatka, M.; Klatka, J.; Błażewicz, A. Specific Lipidomic Shifts in Chronic Lymphocytic Leukemia at Diagnosis. Cancers 2026, 18, 896. https://doi.org/10.3390/cancers18060896Type: Article  |  Publication date: 10 March 2026
Summary: Chronic lymphocytic leukemia (CLL) is a common type of adult blood cancer in which cells survive longer than normal, partly due to changes in how they process fats and other molecules for energy. This study examined the blood plasma of newly diagnosed patients who had not yet received treatment to identify unique patterns in lipid molecules. We found that patients with CLL had higher levels of certain fats, including carnitines and specific phospholipids, compared with healthy individuals. By analyzing these lipid changes using predictive bioinformatics tools, we identified that several pathways involved in lipid metabolism are likely disrupted. These findings improve our understanding of how this disease alters the body’s metabolism and could inform future research on biomarkers for earlier disease detection and treatment development.
Keywords: chronic lymphocytic leukemia (CLL); metabolic reprogramming; carnitines; ether-linked phospholipids; lipidomics

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1261</itunes:duration>
                <itunes:episode>42</itunes:episode>
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            </item>
    <item>
        <title>E40 - Frailty Assessments in Lung Cancer Clinics</title>
        <itunes:title>E40 - Frailty Assessments in Lung Cancer Clinics</itunes:title>
        <link>https://podcast.sinapsos.com/e/e40-frailty-assessments-in-lung-cancer-clinics/</link>
                    <comments>https://podcast.sinapsos.com/e/e40-frailty-assessments-in-lung-cancer-clinics/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:19:15 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/1ee0f72f-bbe0-3c11-a0de-7b59caf0736b</guid>
                                    <description><![CDATA[<p>E40   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/884'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Pearce, J.; Hamzeh, H.; Denholm, M.; Greystoke, A.; Gomes, F.; Clegg, A.; Velikova, G.; Richards, S.H.; Gilbert, A. Clinicians’ Experiences of Implementing Clinical Frailty Scale Assessments in Lung Oncology Clinics: A Qualitative Interview Study. Cancers 2026, 18, 884. https://doi.org/10.3390/cancers18050884
Type: Article  |  Publication date: 09 March 2026

</li>
<li>Summary: Simple frailty assessments, such as the clinical frailty scale (CFS), could support treatment decision-making and care in cancer clinics, but they are not currently used routinely. This qualitative interview study explored clinicians’ experiences of using frailty assessments in lung cancer clinics to understand how they impact care, and the barriers and facilitators to their use. Four main themes were identified. ‘Assessing fitness and frailty’ explores the central role of performance status in assessing fitness and accessing cancer treatments, as well as its limitations and what frailty assessments add. ‘Scoring and interpreting CFS’ describes the ease and relative yield of CFS use, and its ability to differentiate between patients considered ‘borderline’ according to performance status, as well as the need to consider scoring in the wider clinical context. ‘Role of frailty and impacts of assessment’ highlights how frailty assessments can enhance patient-centred care and support, communication with patients, and clinical and shared decision-making, with the potential to streamline care and convey wider system-level benefits. ‘Barriers and facilitators to implementation’ describes factors that help or hinder the delivery of frailty assessments and frailty-informed care, with specific recommendations provided to support use in practice.

</li>
<li>Keywords: frailty; geriatric oncology; qualitative research; frailty assessment; frailty screening; clinical frailty scale (CFS); frailty-informed care</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E40   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/884'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Pearce, J.; Hamzeh, H.; Denholm, M.; Greystoke, A.; Gomes, F.; Clegg, A.; Velikova, G.; Richards, S.H.; Gilbert, A. Clinicians’ Experiences of Implementing Clinical Frailty Scale Assessments in Lung Oncology Clinics: A Qualitative Interview Study. Cancers 2026, 18, 884. https://doi.org/10.3390/cancers18050884<br>
Type: Article  |  Publication date: 09 March 2026<br>
<br>
</li>
<li>Summary: Simple frailty assessments, such as the clinical frailty scale (CFS), could support treatment decision-making and care in cancer clinics, but they are not currently used routinely. This qualitative interview study explored clinicians’ experiences of using frailty assessments in lung cancer clinics to understand how they impact care, and the barriers and facilitators to their use. Four main themes were identified. ‘Assessing fitness and frailty’ explores the central role of performance status in assessing fitness and accessing cancer treatments, as well as its limitations and what frailty assessments add. ‘Scoring and interpreting CFS’ describes the ease and relative yield of CFS use, and its ability to differentiate between patients considered ‘borderline’ according to performance status, as well as the need to consider scoring in the wider clinical context. ‘Role of frailty and impacts of assessment’ highlights how frailty assessments can enhance patient-centred care and support, communication with patients, and clinical and shared decision-making, with the potential to streamline care and convey wider system-level benefits. ‘Barriers and facilitators to implementation’ describes factors that help or hinder the delivery of frailty assessments and frailty-informed care, with specific recommendations provided to support use in practice.<br>
<br>
</li>
<li>Keywords: frailty; geriatric oncology; qualitative research; frailty assessment; frailty screening; clinical frailty scale (CFS); frailty-informed care</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/uvemt6hvsy4a5sg9/E40_-_Frailty_Assessments_in_Lung_Cancer_Clinics.mp3" length="24787321" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E40   |  18 min   |   Latest   |  Publication Link

Podcast based on: Pearce, J.; Hamzeh, H.; Denholm, M.; Greystoke, A.; Gomes, F.; Clegg, A.; Velikova, G.; Richards, S.H.; Gilbert, A. Clinicians’ Experiences of Implementing Clinical Frailty Scale Assessments in Lung Oncology Clinics: A Qualitative Interview Study. Cancers 2026, 18, 884. https://doi.org/10.3390/cancers18050884Type: Article  |  Publication date: 09 March 2026
Summary: Simple frailty assessments, such as the clinical frailty scale (CFS), could support treatment decision-making and care in cancer clinics, but they are not currently used routinely. This qualitative interview study explored clinicians’ experiences of using frailty assessments in lung cancer clinics to understand how they impact care, and the barriers and facilitators to their use. Four main themes were identified. ‘Assessing fitness and frailty’ explores the central role of performance status in assessing fitness and accessing cancer treatments, as well as its limitations and what frailty assessments add. ‘Scoring and interpreting CFS’ describes the ease and relative yield of CFS use, and its ability to differentiate between patients considered ‘borderline’ according to performance status, as well as the need to consider scoring in the wider clinical context. ‘Role of frailty and impacts of assessment’ highlights how frailty assessments can enhance patient-centred care and support, communication with patients, and clinical and shared decision-making, with the potential to streamline care and convey wider system-level benefits. ‘Barriers and facilitators to implementation’ describes factors that help or hinder the delivery of frailty assessments and frailty-informed care, with specific recommendations provided to support use in practice.
Keywords: frailty; geriatric oncology; qualitative research; frailty assessment; frailty screening; clinical frailty scale (CFS); frailty-informed care

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1032</itunes:duration>
                <itunes:episode>41</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E39 - Nutrition in Pediatric Cancer Care</title>
        <itunes:title>E39 - Nutrition in Pediatric Cancer Care</itunes:title>
        <link>https://podcast.sinapsos.com/e/e39-nutrition-in-pediatric-cancer-care/</link>
                    <comments>https://podcast.sinapsos.com/e/e39-nutrition-in-pediatric-cancer-care/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:18:14 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/94ef1131-8d2c-3184-b483-20c67d3f9b62</guid>
                                    <description><![CDATA[<p>E39   |  19 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/873'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Suwannaying, K.; Rujkijyanont, P.; Inaba, H. Nutritional Assessment of Children and Adolescents with Cancer in Various Resource Settings. Cancers 2026, 18, 873. https://doi.org/10.3390/cancers18050873
Type: Review  |  Publication date: 08 March 2026

</li>
<li>Summary: Nutrition has bidirectional effects in children with cancer. It influences, and is influenced by, the disease and treatment, starting from the diagnosis and continuing through therapy into survivorship. Therefore, a longitudinal comprehensive nutritional assessment is essential to define the patient’s nutritional status and to guide management. Assessment strategies should be tailored not only to specific cancer types but also to the available health care resources. In this review, we discuss practical methods for evaluating malnutrition, including their advantages and limitations. We also provide a structured approach for use in various resource settings. This approach will guide nutritional management that can enhance treatment outcomes for children with cancer.

</li>
<li>Keywords: nutrition; assessment; children; cancer; resource-setting</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E39   |  19 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/873'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Suwannaying, K.; Rujkijyanont, P.; Inaba, H. Nutritional Assessment of Children and Adolescents with Cancer in Various Resource Settings. Cancers 2026, 18, 873. https://doi.org/10.3390/cancers18050873<br>
Type: Review  |  Publication date: 08 March 2026<br>
<br>
</li>
<li>Summary: Nutrition has bidirectional effects in children with cancer. It influences, and is influenced by, the disease and treatment, starting from the diagnosis and continuing through therapy into survivorship. Therefore, a longitudinal comprehensive nutritional assessment is essential to define the patient’s nutritional status and to guide management. Assessment strategies should be tailored not only to specific cancer types but also to the available health care resources. In this review, we discuss practical methods for evaluating malnutrition, including their advantages and limitations. We also provide a structured approach for use in various resource settings. This approach will guide nutritional management that can enhance treatment outcomes for children with cancer.<br>
<br>
</li>
<li>Keywords: nutrition; assessment; children; cancer; resource-setting</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/furdsqwr69zq4yha/E39_-_Nutrition_in_Pediatric_Cancer_Care.mp3" length="26307648" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E39   |  19 min   |   Latest   |  Publication Link

Podcast based on: Suwannaying, K.; Rujkijyanont, P.; Inaba, H. Nutritional Assessment of Children and Adolescents with Cancer in Various Resource Settings. Cancers 2026, 18, 873. https://doi.org/10.3390/cancers18050873Type: Review  |  Publication date: 08 March 2026
Summary: Nutrition has bidirectional effects in children with cancer. It influences, and is influenced by, the disease and treatment, starting from the diagnosis and continuing through therapy into survivorship. Therefore, a longitudinal comprehensive nutritional assessment is essential to define the patient’s nutritional status and to guide management. Assessment strategies should be tailored not only to specific cancer types but also to the available health care resources. In this review, we discuss practical methods for evaluating malnutrition, including their advantages and limitations. We also provide a structured approach for use in various resource settings. This approach will guide nutritional management that can enhance treatment outcomes for children with cancer.
Keywords: nutrition; assessment; children; cancer; resource-setting

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1096</itunes:duration>
                <itunes:episode>40</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E38 - mRNA-miRNA Profiling in Ovarian Cancer</title>
        <itunes:title>E38 - mRNA-miRNA Profiling in Ovarian Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e38-mrna-mirna-profiling-in-ovarian-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e38-mrna-mirna-profiling-in-ovarian-cancer/#comments</comments>        <pubDate>Sun, 15 Mar 2026 21:17:13 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/0b0d36e3-ef37-3a07-9449-a22b059a13e6</guid>
                                    <description><![CDATA[<p>E38   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/866'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Hablase, R.; Sisu, C.; Karteris, E.; Chatterjee, J. Integrative In Silico mRNA–miRNA Profiling of mTOR Pathway Dysregulation in High-Grade Serous Ovarian Carcinoma. Cancers 2026, 18, 866. https://doi.org/10.3390/cancers18050866
Type: Article  |  Publication date: 07 March 2026

</li>
<li>Summary: High-grade serous ovarian cancer (HGSOC) is the most common and aggressive type of ovarian cancer. It is often diagnosed at a late stage and eventually becomes resistant to standard chemotherapy. The mechanistic target of rapamycin (mTOR) is a key regulator of cellular functions including growth, survival, immune responses, and metabolism. To show how the mTOR pathway becomes dysregulated in HGSOC, we analysed gene expression data and microRNA patterns from both ovarian cancer patients and healthy individuals. We found that many of the genes involved in the mTOR pathway are unusually dysregulated. A group of regulatory molecules, the let-7 miRNAs, may allow this abnormal activity to continue. We also discovered a distinct pattern where one part of the pathway (mTORC1) is switched on while another (mTORC2) is switched off. These findings may help guide more effective, targeted treatments in the future targeting these pathways.

</li>
<li>Keywords: ovarian cancer; mTOR; TCGA; GTEx; miRNA</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E38   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/866'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Hablase, R.; Sisu, C.; Karteris, E.; Chatterjee, J. Integrative In Silico mRNA–miRNA Profiling of mTOR Pathway Dysregulation in High-Grade Serous Ovarian Carcinoma. Cancers 2026, 18, 866. https://doi.org/10.3390/cancers18050866<br>
Type: Article  |  Publication date: 07 March 2026<br>
<br>
</li>
<li>Summary: High-grade serous ovarian cancer (HGSOC) is the most common and aggressive type of ovarian cancer. It is often diagnosed at a late stage and eventually becomes resistant to standard chemotherapy. The mechanistic target of rapamycin (mTOR) is a key regulator of cellular functions including growth, survival, immune responses, and metabolism. To show how the mTOR pathway becomes dysregulated in HGSOC, we analysed gene expression data and microRNA patterns from both ovarian cancer patients and healthy individuals. We found that many of the genes involved in the mTOR pathway are unusually dysregulated. A group of regulatory molecules, the let-7 miRNAs, may allow this abnormal activity to continue. We also discovered a distinct pattern where one part of the pathway (mTORC1) is switched on while another (mTORC2) is switched off. These findings may help guide more effective, targeted treatments in the future targeting these pathways.<br>
<br>
</li>
<li>Keywords: ovarian cancer; mTOR; TCGA; GTEx; miRNA</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/5u4grsdrnq6trbqc/E38_-_mRNA-miRNA_Profiling_in_Ovarian_Cancer.mp3" length="19668993" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E38   |  14 min   |   Latest   |  Publication Link

Podcast based on: Hablase, R.; Sisu, C.; Karteris, E.; Chatterjee, J. Integrative In Silico mRNA–miRNA Profiling of mTOR Pathway Dysregulation in High-Grade Serous Ovarian Carcinoma. Cancers 2026, 18, 866. https://doi.org/10.3390/cancers18050866Type: Article  |  Publication date: 07 March 2026
Summary: High-grade serous ovarian cancer (HGSOC) is the most common and aggressive type of ovarian cancer. It is often diagnosed at a late stage and eventually becomes resistant to standard chemotherapy. The mechanistic target of rapamycin (mTOR) is a key regulator of cellular functions including growth, survival, immune responses, and metabolism. To show how the mTOR pathway becomes dysregulated in HGSOC, we analysed gene expression data and microRNA patterns from both ovarian cancer patients and healthy individuals. We found that many of the genes involved in the mTOR pathway are unusually dysregulated. A group of regulatory molecules, the let-7 miRNAs, may allow this abnormal activity to continue. We also discovered a distinct pattern where one part of the pathway (mTORC1) is switched on while another (mTORC2) is switched off. These findings may help guide more effective, targeted treatments in the future targeting these pathways.
Keywords: ovarian cancer; mTOR; TCGA; GTEx; miRNA

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>819</itunes:duration>
                <itunes:episode>39</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E37 - Addressing Disparities in Thoracic Oncology Care</title>
        <itunes:title>E37 - Addressing Disparities in Thoracic Oncology Care</itunes:title>
        <link>https://podcast.sinapsos.com/e/e37-addressing-disparities-in-thoracic-oncology-care/</link>
                    <comments>https://podcast.sinapsos.com/e/e37-addressing-disparities-in-thoracic-oncology-care/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:52:39 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/5a214822-1b51-38f2-9751-27c0c12ddff0</guid>
                                    <description><![CDATA[<p>E37   |  16 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/793'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Awlad Mohammad, M.W.; Abu Hashhash, K.; Yacoub, R.; Abu Akar, F. Disparities in Thoracic Oncology Patients. Cancers 2026, 18, 793. https://doi.org/10.3390/cancers18050793
Type: Review  |  Publication date: 28 February 2026

</li>
<li>Summary: Lung cancer continues to be a predominant cause of cancer-related mortality globally; however, not all individuals experience equal advantages from advancements in screening, diagnosis, and treatment. Countless individuals from underprivileged backgrounds face elevated risks, delayed diagnoses, and worse access to adequate healthcare, resulting in adverse consequences. This review aimed to elucidate the impact of social, economic, racial, and geographic determinants on lung cancer along the continuum of care, encompassing risk exposure, early detection, treatment, and survival outcomes. The authors intend to consolidate existing research to elucidate the locations and reasons for these inequalities and their impact on patient outcomes. The results underscore that enhancing lung cancer survival necessitates not only medical advancements but also equitable access to screening, prompt diagnosis, effective treatment, and involvement in research. This study may inform future research, policy, and healthcare practices aimed at achieving equitable lung cancer care for all demographics.

</li>
<li>Keywords: lung cancer; disparities; epidemiology treatment; screening</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E37   |  16 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/793'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Awlad Mohammad, M.W.; Abu Hashhash, K.; Yacoub, R.; Abu Akar, F. Disparities in Thoracic Oncology Patients. Cancers 2026, 18, 793. https://doi.org/10.3390/cancers18050793<br>
Type: Review  |  Publication date: 28 February 2026<br>
<br>
</li>
<li>Summary: Lung cancer continues to be a predominant cause of cancer-related mortality globally; however, not all individuals experience equal advantages from advancements in screening, diagnosis, and treatment. Countless individuals from underprivileged backgrounds face elevated risks, delayed diagnoses, and worse access to adequate healthcare, resulting in adverse consequences. This review aimed to elucidate the impact of social, economic, racial, and geographic determinants on lung cancer along the continuum of care, encompassing risk exposure, early detection, treatment, and survival outcomes. The authors intend to consolidate existing research to elucidate the locations and reasons for these inequalities and their impact on patient outcomes. The results underscore that enhancing lung cancer survival necessitates not only medical advancements but also equitable access to screening, prompt diagnosis, effective treatment, and involvement in research. This study may inform future research, policy, and healthcare practices aimed at achieving equitable lung cancer care for all demographics.<br>
<br>
</li>
<li>Keywords: lung cancer; disparities; epidemiology treatment; screening</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/fimz74h7bq85fa3t/E37_-_Addressing_Disparities_in_Thoracic_Oncology_Care.mp3" length="22250727" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E37   |  16 min   |   Latest   |  Publication Link

Podcast based on: Awlad Mohammad, M.W.; Abu Hashhash, K.; Yacoub, R.; Abu Akar, F. Disparities in Thoracic Oncology Patients. Cancers 2026, 18, 793. https://doi.org/10.3390/cancers18050793Type: Review  |  Publication date: 28 February 2026
Summary: Lung cancer continues to be a predominant cause of cancer-related mortality globally; however, not all individuals experience equal advantages from advancements in screening, diagnosis, and treatment. Countless individuals from underprivileged backgrounds face elevated risks, delayed diagnoses, and worse access to adequate healthcare, resulting in adverse consequences. This review aimed to elucidate the impact of social, economic, racial, and geographic determinants on lung cancer along the continuum of care, encompassing risk exposure, early detection, treatment, and survival outcomes. The authors intend to consolidate existing research to elucidate the locations and reasons for these inequalities and their impact on patient outcomes. The results underscore that enhancing lung cancer survival necessitates not only medical advancements but also equitable access to screening, prompt diagnosis, effective treatment, and involvement in research. This study may inform future research, policy, and healthcare practices aimed at achieving equitable lung cancer care for all demographics.
Keywords: lung cancer; disparities; epidemiology treatment; screening

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>927</itunes:duration>
                <itunes:episode>38</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E36 - ER-Negative Endometrial Cancer Diagnosis and Implications</title>
        <itunes:title>E36 - ER-Negative Endometrial Cancer Diagnosis and Implications</itunes:title>
        <link>https://podcast.sinapsos.com/e/e36-er-negative-endometrial-cancer-diagnosis-and-implications/</link>
                    <comments>https://podcast.sinapsos.com/e/e36-er-negative-endometrial-cancer-diagnosis-and-implications/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:51:55 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/19f840f5-4e64-30e3-a680-f9707725415a</guid>
                                    <description><![CDATA[<p>E36   |  20 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/773'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Fan, R.; Wei, X.; Lea, J.; Zhu, H.; Zheng, W. ER-Negative Endometrial Cancers: An Evolving Diagnostic Category with Major Clinical Implications. Cancers 2026, 18, 773. https://doi.org/10.3390/cancers18050773
Type: Review  |  Publication date: 27 February 2026

</li>
<li>Summary: Estrogen receptor–negative (ER-negative) endometrial carcinomas represent a biologically aggressive and heterogeneous subset of endometrial cancers. Although ER testing has long been used in endometrial carcinoma, it has historically been applied mainly for therapeutic decision-making rather than as a diagnostic tool. Loss of ER expression is associated with poor prognosis but, by itself, is insufficient for accurate tumor classification. In this commentary, we review the evolving diagnostic significance of ER negativity using an integrated framework that incorporates tumor morphology, immunophenotypic features, and molecular heterogeneity. We highlight several high-grade ER-negative tumor types—including gastrointestinal-type adenocarcinoma, pilomatrix-like carcinoma, mesonephric-like adenocarcinoma, clear cell carcinoma, and other high-grade ER-negative carcinomas—that show distinct clinicopathologic characteristics. We propose that ER negativity should be regarded as a diagnostic signal that prompts careful subclassification, with important implications for accurate diagnosis and clinical management.

</li>
<li>Keywords: estrogen receptor–negative (ER-negative) endometrial carcinomas; endometrial gastrointestinal-type adenocarcinoma; pilomatrix-like high-grade endometrial carcinoma; PiMHEC; mesonephric-like adenocarcinoma</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E36   |  20 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/773'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Fan, R.; Wei, X.; Lea, J.; Zhu, H.; Zheng, W. ER-Negative Endometrial Cancers: An Evolving Diagnostic Category with Major Clinical Implications. Cancers 2026, 18, 773. https://doi.org/10.3390/cancers18050773<br>
Type: Review  |  Publication date: 27 February 2026<br>
<br>
</li>
<li>Summary: Estrogen receptor–negative (ER-negative) endometrial carcinomas represent a biologically aggressive and heterogeneous subset of endometrial cancers. Although ER testing has long been used in endometrial carcinoma, it has historically been applied mainly for therapeutic decision-making rather than as a diagnostic tool. Loss of ER expression is associated with poor prognosis but, by itself, is insufficient for accurate tumor classification. In this commentary, we review the evolving diagnostic significance of ER negativity using an integrated framework that incorporates tumor morphology, immunophenotypic features, and molecular heterogeneity. We highlight several high-grade ER-negative tumor types—including gastrointestinal-type adenocarcinoma, pilomatrix-like carcinoma, mesonephric-like adenocarcinoma, clear cell carcinoma, and other high-grade ER-negative carcinomas—that show distinct clinicopathologic characteristics. We propose that ER negativity should be regarded as a diagnostic signal that prompts careful subclassification, with important implications for accurate diagnosis and clinical management.<br>
<br>
</li>
<li>Keywords: estrogen receptor–negative (ER-negative) endometrial carcinomas; endometrial gastrointestinal-type adenocarcinoma; pilomatrix-like high-grade endometrial carcinoma; PiMHEC; mesonephric-like adenocarcinoma</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/eh94am684wake529/E36_-_ER-Negative_Endometrial_Cancer_Diagnosis_and_Implications.mp3" length="28293790" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E36   |  20 min   |   Latest   |  Publication Link

Podcast based on: Fan, R.; Wei, X.; Lea, J.; Zhu, H.; Zheng, W. ER-Negative Endometrial Cancers: An Evolving Diagnostic Category with Major Clinical Implications. Cancers 2026, 18, 773. https://doi.org/10.3390/cancers18050773Type: Review  |  Publication date: 27 February 2026
Summary: Estrogen receptor–negative (ER-negative) endometrial carcinomas represent a biologically aggressive and heterogeneous subset of endometrial cancers. Although ER testing has long been used in endometrial carcinoma, it has historically been applied mainly for therapeutic decision-making rather than as a diagnostic tool. Loss of ER expression is associated with poor prognosis but, by itself, is insufficient for accurate tumor classification. In this commentary, we review the evolving diagnostic significance of ER negativity using an integrated framework that incorporates tumor morphology, immunophenotypic features, and molecular heterogeneity. We highlight several high-grade ER-negative tumor types—including gastrointestinal-type adenocarcinoma, pilomatrix-like carcinoma, mesonephric-like adenocarcinoma, clear cell carcinoma, and other high-grade ER-negative carcinomas—that show distinct clinicopathologic characteristics. We propose that ER negativity should be regarded as a diagnostic signal that prompts careful subclassification, with important implications for accurate diagnosis and clinical management.
Keywords: estrogen receptor–negative (ER-negative) endometrial carcinomas; endometrial gastrointestinal-type adenocarcinoma; pilomatrix-like high-grade endometrial carcinoma; PiMHEC; mesonephric-like adenocarcinoma

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1178</itunes:duration>
                <itunes:episode>37</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E35 - AI-Driven Drug Repurposing for Head and Neck Cancer</title>
        <itunes:title>E35 - AI-Driven Drug Repurposing for Head and Neck Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e35-ai-driven-drug-repurposing-for-head-and-neck-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e35-ai-driven-drug-repurposing-for-head-and-neck-cancer/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:51:11 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/8f0ad9e9-ac69-3a80-ad5d-dee9de43bf62</guid>
                                    <description><![CDATA[<p>E35   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/757'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Tanikella, P.; Nenad, W.; Courtine, C.; Dai, Y.; Deng, Q.; Zou, B.; Osazuwa-Peters, N.; Schrank, T.P.; Wu, D. GARD: Genomic Data-Based Drug Repurposing in Head and Neck Cancer with Large Language Model Validation. Cancers 2026, 18, 757. https://doi.org/10.3390/cancers18050757
Type: Article  |  Publication date: 26 February 2026

</li>
<li>Summary: Head and neck cancer (HNC) is among the most prevalent and challenging cancers worldwide. Developing new drugs is expensive and time consuming, so this study explored a faster, cost-effective approach utilizing existing medications with established safety profiles: drug repurposing. We developed the GARDpipeline (Genomic Alteration-based Repurposing for Drugs), which utilizes large-scale genomic data from The Cancer Genome Atlas (TCGA) to identify key genomic changes in HNC. These genes are expanded through protein–protein interaction networks to capture related pathways and then validated using evidence from thousands of PubMed articles extracted by large language model (LLM) tools. Finally, validated genes are matched with drugs using the DrugBank database. This approach uncovered both known cancer drugs and promising new candidates. These included targeted therapies such as Fostamatinib, Nintedanib, Brigatinib, Regorafenib, and Lenvatinib, as well as emerging compounds like Artenimol, Quercetin, and Acetylsalicylic Acid (Aspirin). Through a combination of genomic analysis, network expansion, and literature validation, the GARD pipeline offers a powerful way to accelerate personalized cancer treatments while reducing cost and development time.

</li>
<li>Keywords: head and neck cancer; drug repurposing; genomics</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E35   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/757'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Tanikella, P.; Nenad, W.; Courtine, C.; Dai, Y.; Deng, Q.; Zou, B.; Osazuwa-Peters, N.; Schrank, T.P.; Wu, D. GARD: Genomic Data-Based Drug Repurposing in Head and Neck Cancer with Large Language Model Validation. Cancers 2026, 18, 757. https://doi.org/10.3390/cancers18050757<br>
Type: Article  |  Publication date: 26 February 2026<br>
<br>
</li>
<li>Summary: Head and neck cancer (HNC) is among the most prevalent and challenging cancers worldwide. Developing new drugs is expensive and time consuming, so this study explored a faster, cost-effective approach utilizing existing medications with established safety profiles: drug repurposing. We developed the GARDpipeline (Genomic Alteration-based Repurposing for Drugs), which utilizes large-scale genomic data from The Cancer Genome Atlas (TCGA) to identify key genomic changes in HNC. These genes are expanded through protein–protein interaction networks to capture related pathways and then validated using evidence from thousands of PubMed articles extracted by large language model (LLM) tools. Finally, validated genes are matched with drugs using the DrugBank database. This approach uncovered both known cancer drugs and promising new candidates. These included targeted therapies such as Fostamatinib, Nintedanib, Brigatinib, Regorafenib, and Lenvatinib, as well as emerging compounds like Artenimol, Quercetin, and Acetylsalicylic Acid (Aspirin). Through a combination of genomic analysis, network expansion, and literature validation, the GARD pipeline offers a powerful way to accelerate personalized cancer treatments while reducing cost and development time.<br>
<br>
</li>
<li>Keywords: head and neck cancer; drug repurposing; genomics</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/jjx3u7ch7sxuak3b/E35_-_AI-Driven_Drug_Repurposing_for_Head_and_Neck_Cancer.mp3" length="25492627" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E35   |  18 min   |   Latest   |  Publication Link

Podcast based on: Tanikella, P.; Nenad, W.; Courtine, C.; Dai, Y.; Deng, Q.; Zou, B.; Osazuwa-Peters, N.; Schrank, T.P.; Wu, D. GARD: Genomic Data-Based Drug Repurposing in Head and Neck Cancer with Large Language Model Validation. Cancers 2026, 18, 757. https://doi.org/10.3390/cancers18050757Type: Article  |  Publication date: 26 February 2026
Summary: Head and neck cancer (HNC) is among the most prevalent and challenging cancers worldwide. Developing new drugs is expensive and time consuming, so this study explored a faster, cost-effective approach utilizing existing medications with established safety profiles: drug repurposing. We developed the GARDpipeline (Genomic Alteration-based Repurposing for Drugs), which utilizes large-scale genomic data from The Cancer Genome Atlas (TCGA) to identify key genomic changes in HNC. These genes are expanded through protein–protein interaction networks to capture related pathways and then validated using evidence from thousands of PubMed articles extracted by large language model (LLM) tools. Finally, validated genes are matched with drugs using the DrugBank database. This approach uncovered both known cancer drugs and promising new candidates. These included targeted therapies such as Fostamatinib, Nintedanib, Brigatinib, Regorafenib, and Lenvatinib, as well as emerging compounds like Artenimol, Quercetin, and Acetylsalicylic Acid (Aspirin). Through a combination of genomic analysis, network expansion, and literature validation, the GARD pipeline offers a powerful way to accelerate personalized cancer treatments while reducing cost and development time.
Keywords: head and neck cancer; drug repurposing; genomics

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1062</itunes:duration>
                <itunes:episode>36</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E34 - Managing Toxicities in GEP-NETs After Radioligand Therapy</title>
        <itunes:title>E34 - Managing Toxicities in GEP-NETs After Radioligand Therapy</itunes:title>
        <link>https://podcast.sinapsos.com/e/e34-managing-toxicities-in-gep-nets-after-radioligand-therapy/</link>
                    <comments>https://podcast.sinapsos.com/e/e34-managing-toxicities-in-gep-nets-after-radioligand-therapy/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:50:26 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/ba3b05e3-c2ab-3413-be1a-88d2e6b66999</guid>
                                    <description><![CDATA[<p>E34   |  21 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/742'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: El-Haddad, G.; Gardner, L.; Kim, H.; Soares, H.P. Occurrence and Management of Acute, Subacute, and Delayed Toxicities in Patients with GEP-NETs Following Treatment with Radioligand Therapy. Cancers 2026, 18, 742. https://doi.org/10.3390/cancers18050742
Type: Review  |  Publication date: 25 February 2026

</li>
<li>Summary: Radioligand therapy is a type of treatment being developed for many cancer types, including gastroenteropancreatic neuroendocrine tumors (GEP-NETs). It uses specially designed drugs to deliver radiation directly to tumor cells within the body. Studies have shown that radioligand therapies can help some patients with GEP-NETs to live longer without disease progression. However, side effects have been reported in patients treated with radioligand therapies. Additionally, there is a risk of radiation exposure among people who come into contact with treated patients. In this article, we provide practical strategies to prevent and manage the side effects of radioligand therapy and to maintain radiation safety.

</li>
<li>Keywords: radioligand therapy; gastroenteropancreatic neuroendocrine tumors; adverse event; toxicity; management; radioactive contamination; radiation safety</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E34   |  21 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/742'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: El-Haddad, G.; Gardner, L.; Kim, H.; Soares, H.P. Occurrence and Management of Acute, Subacute, and Delayed Toxicities in Patients with GEP-NETs Following Treatment with Radioligand Therapy. Cancers 2026, 18, 742. https://doi.org/10.3390/cancers18050742<br>
Type: Review  |  Publication date: 25 February 2026<br>
<br>
</li>
<li>Summary: Radioligand therapy is a type of treatment being developed for many cancer types, including gastroenteropancreatic neuroendocrine tumors (GEP-NETs). It uses specially designed drugs to deliver radiation directly to tumor cells within the body. Studies have shown that radioligand therapies can help some patients with GEP-NETs to live longer without disease progression. However, side effects have been reported in patients treated with radioligand therapies. Additionally, there is a risk of radiation exposure among people who come into contact with treated patients. In this article, we provide practical strategies to prevent and manage the side effects of radioligand therapy and to maintain radiation safety.<br>
<br>
</li>
<li>Keywords: radioligand therapy; gastroenteropancreatic neuroendocrine tumors; adverse event; toxicity; management; radioactive contamination; radiation safety</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/a6z25ns4ehpd69y2/E34_-_Managing_Toxicities_in_GEP-NETs_After_Radioligand_Therapy.mp3" length="29980255" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E34   |  21 min   |   Latest   |  Publication Link

Podcast based on: El-Haddad, G.; Gardner, L.; Kim, H.; Soares, H.P. Occurrence and Management of Acute, Subacute, and Delayed Toxicities in Patients with GEP-NETs Following Treatment with Radioligand Therapy. Cancers 2026, 18, 742. https://doi.org/10.3390/cancers18050742Type: Review  |  Publication date: 25 February 2026
Summary: Radioligand therapy is a type of treatment being developed for many cancer types, including gastroenteropancreatic neuroendocrine tumors (GEP-NETs). It uses specially designed drugs to deliver radiation directly to tumor cells within the body. Studies have shown that radioligand therapies can help some patients with GEP-NETs to live longer without disease progression. However, side effects have been reported in patients treated with radioligand therapies. Additionally, there is a risk of radiation exposure among people who come into contact with treated patients. In this article, we provide practical strategies to prevent and manage the side effects of radioligand therapy and to maintain radiation safety.
Keywords: radioligand therapy; gastroenteropancreatic neuroendocrine tumors; adverse event; toxicity; management; radioactive contamination; radiation safety

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1249</itunes:duration>
                <itunes:episode>35</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E33 - Biopsy Tumor Burden vs AI in Prostate Cancer Grading</title>
        <itunes:title>E33 - Biopsy Tumor Burden vs AI in Prostate Cancer Grading</itunes:title>
        <link>https://podcast.sinapsos.com/e/e33-biopsy-tumor-burden-vs-ai-in-prostate-cancer-grading/</link>
                    <comments>https://podcast.sinapsos.com/e/e33-biopsy-tumor-burden-vs-ai-in-prostate-cancer-grading/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:49:42 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/e5843e99-cb3d-3235-890e-24c2ead3b1c0</guid>
                                    <description><![CDATA[<p>E33   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/730'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Condoiu, C.; Baloi, A.; Sandesc, D.; Cumpanas, A.A.; Latcu, S.; Dema, V.; Caprariu, R.; Barb, A.C.; Ciucurita, A.; Marinescu, A.; Cut, T.G.; Bardan, R. Clinically Significant ISUP Upgrading in the Multiparametric MRI Era: Biopsy Tumor Burden Outperforms Complex Machine Learning Models in a Single-Center Exploratory Cohort. Cancers 2026, 18, 730. https://doi.org/10.3390/cancers18050730
Type: Article  |  Publication date: 24 February 2026

</li>
<li>Summary: Sometimes, a prostate biopsy underestimates how aggressive the cancer is. This study looked at ways to predict when the final surgery will find a higher-grade cancer than the initial biopsy. We analyzed 96 men who had both a biopsy and their prostate removed. We focused on factors like PSA (a blood test for prostate cancer), MRI scans, and biopsy results. We found that the extent of cancer involvement in biopsy cores, and to a lesser degree PSA density, were associated with upgrading risk to a more aggressive cancer at surgery. Using just these two factors, a simple statistical model predicted grade upgrading more accurately than more complex computer models. If confirmed in larger studies, this tool could help doctors identify patients who have more aggressive cancer than initially thought, so they can choose the best treatment.

</li>
<li>Keywords: prostate cancer; precision medicine; artificial intelligence; personalized treatment; imaging modalities; risk stratification; ISUP upgrading; PSA density; positive core ratio; multiparametric MRI</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E33   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/5/730'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Condoiu, C.; Baloi, A.; Sandesc, D.; Cumpanas, A.A.; Latcu, S.; Dema, V.; Caprariu, R.; Barb, A.C.; Ciucurita, A.; Marinescu, A.; Cut, T.G.; Bardan, R. Clinically Significant ISUP Upgrading in the Multiparametric MRI Era: Biopsy Tumor Burden Outperforms Complex Machine Learning Models in a Single-Center Exploratory Cohort. Cancers 2026, 18, 730. https://doi.org/10.3390/cancers18050730<br>
Type: Article  |  Publication date: 24 February 2026<br>
<br>
</li>
<li>Summary: Sometimes, a prostate biopsy underestimates how aggressive the cancer is. This study looked at ways to predict when the final surgery will find a higher-grade cancer than the initial biopsy. We analyzed 96 men who had both a biopsy and their prostate removed. We focused on factors like PSA (a blood test for prostate cancer), MRI scans, and biopsy results. We found that the extent of cancer involvement in biopsy cores, and to a lesser degree PSA density, were associated with upgrading risk to a more aggressive cancer at surgery. Using just these two factors, a simple statistical model predicted grade upgrading more accurately than more complex computer models. If confirmed in larger studies, this tool could help doctors identify patients who have more aggressive cancer than initially thought, so they can choose the best treatment.<br>
<br>
</li>
<li>Keywords: prostate cancer; precision medicine; artificial intelligence; personalized treatment; imaging modalities; risk stratification; ISUP upgrading; PSA density; positive core ratio; multiparametric MRI</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/d79xjazb6zmg27h9/E33_-_Biopsy_Tumor_Burden_vs_AI_in_Prostate_Cancer_Grading.mp3" length="19998136" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E33   |  14 min   |   Latest   |  Publication Link

Podcast based on: Condoiu, C.; Baloi, A.; Sandesc, D.; Cumpanas, A.A.; Latcu, S.; Dema, V.; Caprariu, R.; Barb, A.C.; Ciucurita, A.; Marinescu, A.; Cut, T.G.; Bardan, R. Clinically Significant ISUP Upgrading in the Multiparametric MRI Era: Biopsy Tumor Burden Outperforms Complex Machine Learning Models in a Single-Center Exploratory Cohort. Cancers 2026, 18, 730. https://doi.org/10.3390/cancers18050730Type: Article  |  Publication date: 24 February 2026
Summary: Sometimes, a prostate biopsy underestimates how aggressive the cancer is. This study looked at ways to predict when the final surgery will find a higher-grade cancer than the initial biopsy. We analyzed 96 men who had both a biopsy and their prostate removed. We focused on factors like PSA (a blood test for prostate cancer), MRI scans, and biopsy results. We found that the extent of cancer involvement in biopsy cores, and to a lesser degree PSA density, were associated with upgrading risk to a more aggressive cancer at surgery. Using just these two factors, a simple statistical model predicted grade upgrading more accurately than more complex computer models. If confirmed in larger studies, this tool could help doctors identify patients who have more aggressive cancer than initially thought, so they can choose the best treatment.
Keywords: prostate cancer; precision medicine; artificial intelligence; personalized treatment; imaging modalities; risk stratification; ISUP upgrading; PSA density; positive core ratio; multiparametric MRI

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>833</itunes:duration>
                <itunes:episode>34</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E32 - Biomarkers for Immunotherapy Response in Kidney Cancer</title>
        <itunes:title>E32 - Biomarkers for Immunotherapy Response in Kidney Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e32-biomarkers-for-immunotherapy-response-in-kidney-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e32-biomarkers-for-immunotherapy-response-in-kidney-cancer/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:48:58 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/8b52a2a2-aa3d-3e8c-b4f8-75cf19b0a5d5</guid>
                                    <description><![CDATA[<p>E32   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/716'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Katifelis, H.; Zerva, S.; Bamias, A.; Karamouzis, M.V.; Stravodimos, K.; Sechi, L.A.; Lampropoulou, D.; Pliakou, E.; Gazouli, M. Circulating ERVFRD-1 and MFSD2A Are Associated with Immunotherapy Response in Metastatic Clear Cell Renal Cell Carcinoma. Cancers 2026, 18, 716. https://doi.org/10.3390/cancers18040716
Type: Article  |  Publication date: 23 February 2026

</li>
<li>Summary: Immune checkpoint inhibitor (ICI) therapies have improved outcomes for patients with metastatic clear cell renal cell carcinoma (mccRCC). However, many patients do not respond to treatment. Therefore, reliable biomarkers associated with therapeutic response are urgently needed. Blood-based biomarkers offer a non-invasive alternative to tissue analysis. In this study, we investigated the expression of two immunity-related genes, ERVFRD-1 and MFSD2A, in peripheral blood samples from mccRCC patients receiving PD-1-based treatment. Both genes were dysregulated compared with healthy controls and demonstrated differential baseline expression between patients who achieved clinical benefit and those with progressive disease. Patients with progressive disease exhibited decreased expression of ERVFRD-1 and increased expression of MFSD2A. These findings suggest that ERVFRD-1 and MFSD2A may serve as candidate blood-based biomarkers associated with response to ICI, although confirmation in larger prospective studies is required.

</li>
<li>Keywords: ccRCC; immunotherapy; ICIs; PD-1; TKI; ;</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E32   |  18 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/716'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Katifelis, H.; Zerva, S.; Bamias, A.; Karamouzis, M.V.; Stravodimos, K.; Sechi, L.A.; Lampropoulou, D.; Pliakou, E.; Gazouli, M. Circulating ERVFRD-1 and MFSD2A Are Associated with Immunotherapy Response in Metastatic Clear Cell Renal Cell Carcinoma. Cancers 2026, 18, 716. https://doi.org/10.3390/cancers18040716<br>
Type: Article  |  Publication date: 23 February 2026<br>
<br>
</li>
<li>Summary: Immune checkpoint inhibitor (ICI) therapies have improved outcomes for patients with metastatic clear cell renal cell carcinoma (mccRCC). However, many patients do not respond to treatment. Therefore, reliable biomarkers associated with therapeutic response are urgently needed. Blood-based biomarkers offer a non-invasive alternative to tissue analysis. In this study, we investigated the expression of two immunity-related genes, ERVFRD-1 and MFSD2A, in peripheral blood samples from mccRCC patients receiving PD-1-based treatment. Both genes were dysregulated compared with healthy controls and demonstrated differential baseline expression between patients who achieved clinical benefit and those with progressive disease. Patients with progressive disease exhibited decreased expression of ERVFRD-1 and increased expression of MFSD2A. These findings suggest that ERVFRD-1 and MFSD2A may serve as candidate blood-based biomarkers associated with response to ICI, although confirmation in larger prospective studies is required.<br>
<br>
</li>
<li>Keywords: ccRCC; immunotherapy; ICIs; PD-1; TKI; ;</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/7q3u3suecssy8ndd/E32_-_Biomarkers_for_Immunotherapy_Response_in_Kidney_Cancer.mp3" length="25357208" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E32   |  18 min   |   Latest   |  Publication Link

Podcast based on: Katifelis, H.; Zerva, S.; Bamias, A.; Karamouzis, M.V.; Stravodimos, K.; Sechi, L.A.; Lampropoulou, D.; Pliakou, E.; Gazouli, M. Circulating ERVFRD-1 and MFSD2A Are Associated with Immunotherapy Response in Metastatic Clear Cell Renal Cell Carcinoma. Cancers 2026, 18, 716. https://doi.org/10.3390/cancers18040716Type: Article  |  Publication date: 23 February 2026
Summary: Immune checkpoint inhibitor (ICI) therapies have improved outcomes for patients with metastatic clear cell renal cell carcinoma (mccRCC). However, many patients do not respond to treatment. Therefore, reliable biomarkers associated with therapeutic response are urgently needed. Blood-based biomarkers offer a non-invasive alternative to tissue analysis. In this study, we investigated the expression of two immunity-related genes, ERVFRD-1 and MFSD2A, in peripheral blood samples from mccRCC patients receiving PD-1-based treatment. Both genes were dysregulated compared with healthy controls and demonstrated differential baseline expression between patients who achieved clinical benefit and those with progressive disease. Patients with progressive disease exhibited decreased expression of ERVFRD-1 and increased expression of MFSD2A. These findings suggest that ERVFRD-1 and MFSD2A may serve as candidate blood-based biomarkers associated with response to ICI, although confirmation in larger prospective studies is required.
Keywords: ccRCC; immunotherapy; ICIs; PD-1; TKI; ;

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1056</itunes:duration>
                <itunes:episode>33</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E31 - TIC TOC Trial Cell Salvage vs Transfusion in Ovarian Cancer</title>
        <itunes:title>E31 - TIC TOC Trial Cell Salvage vs Transfusion in Ovarian Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e31-tic-toc-trial-cell-salvage-vs-transfusion-in-ovarian-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e31-tic-toc-trial-cell-salvage-vs-transfusion-in-ovarian-cancer/#comments</comments>        <pubDate>Mon, 02 Mar 2026 14:48:14 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/41b99ac4-5a21-3755-830d-01a6c6e57235</guid>
                                    <description><![CDATA[<p>E31   |  17 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/711'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Galaal, K.; Vickery, P.J.; Marques, E.; Palmer, J.; Jones, B.; O’Shaughnessy, E.; Lopes, A.; Ewings, P.; Bekkers, R.L.M. The Trial of Intraoperative Cell Salvage Versus Transfusion in Ovarian Cancer (TIC TOC): Results of a Randomized Controlled Feasibility Study. Cancers 2026, 18, 711. https://doi.org/10.3390/cancers18040711
Type: Article  |  Publication date: 22 February 2026

</li>
<li>Summary: This study looked at whether it is acceptable to use intraoperative cell salvage (ICS) during surgery for women with advanced (stage 3–4) ovarian cancer. ICS is a method that collects a patient’s own blood lost during surgery, cleans it, and gives it back to them, reducing the need for donated blood. A total of 57 women with ovarian cancer took part; the amount of blood loss during surgery was similar in both groups. In the ICS group, about two-thirds of the women who had surgery received their own salvaged blood. Women appeared comfortable with the idea of receiving their own salvaged blood. Overall, this study shows that using ICS in ovarian cancer surgery is both feasible and acceptable to patients. The findings suggest that a larger trial should now be carried out to determine whether ICS can reduce the need for donor blood and improve patient outcomes.

</li>
<li>Keywords: intraoperative cell salvage; blood transfusion; cytoreductive surgery; ovarian cancer; randomized feasibility trial</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E31   |  17 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/711'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Galaal, K.; Vickery, P.J.; Marques, E.; Palmer, J.; Jones, B.; O’Shaughnessy, E.; Lopes, A.; Ewings, P.; Bekkers, R.L.M. The Trial of Intraoperative Cell Salvage Versus Transfusion in Ovarian Cancer (TIC TOC): Results of a Randomized Controlled Feasibility Study. Cancers 2026, 18, 711. https://doi.org/10.3390/cancers18040711<br>
Type: Article  |  Publication date: 22 February 2026<br>
<br>
</li>
<li>Summary: This study looked at whether it is acceptable to use intraoperative cell salvage (ICS) during surgery for women with advanced (stage 3–4) ovarian cancer. ICS is a method that collects a patient’s own blood lost during surgery, cleans it, and gives it back to them, reducing the need for donated blood. A total of 57 women with ovarian cancer took part; the amount of blood loss during surgery was similar in both groups. In the ICS group, about two-thirds of the women who had surgery received their own salvaged blood. Women appeared comfortable with the idea of receiving their own salvaged blood. Overall, this study shows that using ICS in ovarian cancer surgery is both feasible and acceptable to patients. The findings suggest that a larger trial should now be carried out to determine whether ICS can reduce the need for donor blood and improve patient outcomes.<br>
<br>
</li>
<li>Keywords: intraoperative cell salvage; blood transfusion; cytoreductive surgery; ovarian cancer; randomized feasibility trial</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/c6yyvhrdn8k5vgs2/E31_-_TIC_TOC_Trial_Cell_Salvage_vs_Transfusion_in_Ovarian_Canc.mp3" length="24200506" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E31   |  17 min   |   Latest   |  Publication Link

Podcast based on: Galaal, K.; Vickery, P.J.; Marques, E.; Palmer, J.; Jones, B.; O’Shaughnessy, E.; Lopes, A.; Ewings, P.; Bekkers, R.L.M. The Trial of Intraoperative Cell Salvage Versus Transfusion in Ovarian Cancer (TIC TOC): Results of a Randomized Controlled Feasibility Study. Cancers 2026, 18, 711. https://doi.org/10.3390/cancers18040711Type: Article  |  Publication date: 22 February 2026
Summary: This study looked at whether it is acceptable to use intraoperative cell salvage (ICS) during surgery for women with advanced (stage 3–4) ovarian cancer. ICS is a method that collects a patient’s own blood lost during surgery, cleans it, and gives it back to them, reducing the need for donated blood. A total of 57 women with ovarian cancer took part; the amount of blood loss during surgery was similar in both groups. In the ICS group, about two-thirds of the women who had surgery received their own salvaged blood. Women appeared comfortable with the idea of receiving their own salvaged blood. Overall, this study shows that using ICS in ovarian cancer surgery is both feasible and acceptable to patients. The findings suggest that a larger trial should now be carried out to determine whether ICS can reduce the need for donor blood and improve patient outcomes.
Keywords: intraoperative cell salvage; blood transfusion; cytoreductive surgery; ovarian cancer; randomized feasibility trial

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>1008</itunes:duration>
                <itunes:episode>32</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E30 - Automating Cancer Pain Assessment</title>
        <itunes:title>E30 - Automating Cancer Pain Assessment</itunes:title>
        <link>https://podcast.sinapsos.com/e/e30-automating-cancer-pain-assessment/</link>
                    <comments>https://podcast.sinapsos.com/e/e30-automating-cancer-pain-assessment/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:10:02 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/1695e85d-c73f-3196-b612-4eef5e3a5013</guid>
                                    <description><![CDATA[<p>E30   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/646'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Cascella, M.; Perri, F.; Ottaiano, A.; Santorsola, M.; Marciano, M.L.; Rampetta, F.R.; Pontone, M.; Crispo, A.; Sabbatino, F.; Franci, G.; Esposito, W.; Cisale, G.; Romano, M.; Amato, F.; Scuotto, A.; Santoriello, V.; Ponsiglione, A.M. Linking Cancer Pain Features and Biosignals for Automatic Pain Assessment. Cancers 2026, 18, 646. https://doi.org/10.3390/cancers18040646
Type: Article  |  Publication date: 16 February 2026

</li>
<li>Summary: Although pain is a frequent and burdensome symptom in people with cancer, it is commonly evaluated using self-reported scales that may be unreliable in patients with cognitive, communicative, or clinical limitations. This study explored whether objective physiological signals could enhance cancer pain assessment. We analyzed electrodermal activity and heart rate variability recorded in cancer patients and examined their relationships with pain intensity and pain type. The results indicate that specific electrodermal activity parameters are associated with both pain intensity and distinct pain phenotypes (mainly mixed pain). In contrast, heart rate variability failed to provide meaningful discrimination in this context. Despite limitations, these findings suggest that electrodermal activity may represent a valuable objective marker to complement conventional pain scales and support the development of automated pain assessment approaches in oncology.

</li>
<li>Keywords: cancer pain; breakthrough cancer pain; biosignals; electrodermal activity; automatic pain assessment; heart rate variability</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E30   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/646'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Cascella, M.; Perri, F.; Ottaiano, A.; Santorsola, M.; Marciano, M.L.; Rampetta, F.R.; Pontone, M.; Crispo, A.; Sabbatino, F.; Franci, G.; Esposito, W.; Cisale, G.; Romano, M.; Amato, F.; Scuotto, A.; Santoriello, V.; Ponsiglione, A.M. Linking Cancer Pain Features and Biosignals for Automatic Pain Assessment. Cancers 2026, 18, 646. https://doi.org/10.3390/cancers18040646<br>
Type: Article  |  Publication date: 16 February 2026<br>
<br>
</li>
<li>Summary: Although pain is a frequent and burdensome symptom in people with cancer, it is commonly evaluated using self-reported scales that may be unreliable in patients with cognitive, communicative, or clinical limitations. This study explored whether objective physiological signals could enhance cancer pain assessment. We analyzed electrodermal activity and heart rate variability recorded in cancer patients and examined their relationships with pain intensity and pain type. The results indicate that specific electrodermal activity parameters are associated with both pain intensity and distinct pain phenotypes (mainly mixed pain). In contrast, heart rate variability failed to provide meaningful discrimination in this context. Despite limitations, these findings suggest that electrodermal activity may represent a valuable objective marker to complement conventional pain scales and support the development of automated pain assessment approaches in oncology.<br>
<br>
</li>
<li>Keywords: cancer pain; breakthrough cancer pain; biosignals; electrodermal activity; automatic pain assessment; heart rate variability</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/kfaw23zqy2t474tn/E30_-_Automating_Cancer_Pain_Assessment.mp3" length="14947517" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E30   |  11 min   |   Latest   |  Publication Link

Podcast based on: Cascella, M.; Perri, F.; Ottaiano, A.; Santorsola, M.; Marciano, M.L.; Rampetta, F.R.; Pontone, M.; Crispo, A.; Sabbatino, F.; Franci, G.; Esposito, W.; Cisale, G.; Romano, M.; Amato, F.; Scuotto, A.; Santoriello, V.; Ponsiglione, A.M. Linking Cancer Pain Features and Biosignals for Automatic Pain Assessment. Cancers 2026, 18, 646. https://doi.org/10.3390/cancers18040646Type: Article  |  Publication date: 16 February 2026
Summary: Although pain is a frequent and burdensome symptom in people with cancer, it is commonly evaluated using self-reported scales that may be unreliable in patients with cognitive, communicative, or clinical limitations. This study explored whether objective physiological signals could enhance cancer pain assessment. We analyzed electrodermal activity and heart rate variability recorded in cancer patients and examined their relationships with pain intensity and pain type. The results indicate that specific electrodermal activity parameters are associated with both pain intensity and distinct pain phenotypes (mainly mixed pain). In contrast, heart rate variability failed to provide meaningful discrimination in this context. Despite limitations, these findings suggest that electrodermal activity may represent a valuable objective marker to complement conventional pain scales and support the development of automated pain assessment approaches in oncology.
Keywords: cancer pain; breakthrough cancer pain; biosignals; electrodermal activity; automatic pain assessment; heart rate variability

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
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        <itunes:block>No</itunes:block>
        <itunes:duration>622</itunes:duration>
                <itunes:episode>31</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E29 - Menin Inhibition New Target for Leukemia</title>
        <itunes:title>E29 - Menin Inhibition New Target for Leukemia</itunes:title>
        <link>https://podcast.sinapsos.com/e/e29-menin-inhibition-new-target-for-leukemia/</link>
                    <comments>https://podcast.sinapsos.com/e/e29-menin-inhibition-new-target-for-leukemia/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:09:17 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/5a23d9af-b021-35ad-ab80-7b185fcb0f85</guid>
                                    <description><![CDATA[<p>E29   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/637'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Alati, C.; Molica, M.; Pitea, M.; Marafioti, V.; Porto, G.; Policastro, G.; Bilardi, E.; Utano, G.; Giordano, L.; Sgarlata, A.; Delfino, I.M.; Idato, A.; Santoro, G.; Rossi, M.; Martino, M. Menin Inhibition in Acute Myeloid MLL Rearranged Leukemias: A New Target for Precision Care. Cancers 2026, 18, 637. https://doi.org/10.3390/cancers18040637
Type: Review  |  Publication date: 15 February 2026

</li>
<li>Summary: Menin inhibitors are new targeted drugs for two high-risk types of acute leukemia (KMT2A-rearranged and NPM1-mutated). Revumenib was approved in 2024–2025. In heavily pretreated patients, about 23% achieved complete remission, with most of those becoming MRD-negative. Ziftomenib, bleximenib, and enzomenib show similar effectiveness but differ in side effects, particularly heart rhythm problems (QTc prolongation varies among drugs). When combined with other drugs like azacitidine/venetoclax or chemotherapy, response rates are much higher in newly diagnosed patients, suggesting these could work as initial treatment. About 40% of patients develop resistance, usually through MEN1 gene mutations. Different menin inhibitors have different resistance patterns, so switching drugs might help. About 30–40% of responders went on to stem cell transplant, which remains the best chance for cure. Menin inhibitors are the first targeted therapies for these aggressive leukemias, showing promise both alone and in combinations, though resistance remains a challenge.

</li>
<li>Keywords: menin inhibitors; KMT2A rearrangements; MLL rearrangements; NPM1 mutations; acute myeloid leukemia; revumenib; precision medicine; targeted therapy</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E29   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/637'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Alati, C.; Molica, M.; Pitea, M.; Marafioti, V.; Porto, G.; Policastro, G.; Bilardi, E.; Utano, G.; Giordano, L.; Sgarlata, A.; Delfino, I.M.; Idato, A.; Santoro, G.; Rossi, M.; Martino, M. Menin Inhibition in Acute Myeloid MLL Rearranged Leukemias: A New Target for Precision Care. Cancers 2026, 18, 637. https://doi.org/10.3390/cancers18040637<br>
Type: Review  |  Publication date: 15 February 2026<br>
<br>
</li>
<li>Summary: Menin inhibitors are new targeted drugs for two high-risk types of acute leukemia (KMT2A-rearranged and NPM1-mutated). Revumenib was approved in 2024–2025. In heavily pretreated patients, about 23% achieved complete remission, with most of those becoming MRD-negative. Ziftomenib, bleximenib, and enzomenib show similar effectiveness but differ in side effects, particularly heart rhythm problems (QTc prolongation varies among drugs). When combined with other drugs like azacitidine/venetoclax or chemotherapy, response rates are much higher in newly diagnosed patients, suggesting these could work as initial treatment. About 40% of patients develop resistance, usually through MEN1 gene mutations. Different menin inhibitors have different resistance patterns, so switching drugs might help. About 30–40% of responders went on to stem cell transplant, which remains the best chance for cure. Menin inhibitors are the first targeted therapies for these aggressive leukemias, showing promise both alone and in combinations, though resistance remains a challenge.<br>
<br>
</li>
<li>Keywords: menin inhibitors; KMT2A rearrangements; MLL rearrangements; NPM1 mutations; acute myeloid leukemia; revumenib; precision medicine; targeted therapy</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/x3u3bnbh859j5uvy/E29_-_Menin_Inhibition_New_Target_for_Leukemia.mp3" length="15987608" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E29   |  12 min   |   Latest   |  Publication Link

Podcast based on: Alati, C.; Molica, M.; Pitea, M.; Marafioti, V.; Porto, G.; Policastro, G.; Bilardi, E.; Utano, G.; Giordano, L.; Sgarlata, A.; Delfino, I.M.; Idato, A.; Santoro, G.; Rossi, M.; Martino, M. Menin Inhibition in Acute Myeloid MLL Rearranged Leukemias: A New Target for Precision Care. Cancers 2026, 18, 637. https://doi.org/10.3390/cancers18040637Type: Review  |  Publication date: 15 February 2026
Summary: Menin inhibitors are new targeted drugs for two high-risk types of acute leukemia (KMT2A-rearranged and NPM1-mutated). Revumenib was approved in 2024–2025. In heavily pretreated patients, about 23% achieved complete remission, with most of those becoming MRD-negative. Ziftomenib, bleximenib, and enzomenib show similar effectiveness but differ in side effects, particularly heart rhythm problems (QTc prolongation varies among drugs). When combined with other drugs like azacitidine/venetoclax or chemotherapy, response rates are much higher in newly diagnosed patients, suggesting these could work as initial treatment. About 40% of patients develop resistance, usually through MEN1 gene mutations. Different menin inhibitors have different resistance patterns, so switching drugs might help. About 30–40% of responders went on to stem cell transplant, which remains the best chance for cure. Menin inhibitors are the first targeted therapies for these aggressive leukemias, showing promise both alone and in combinations, though resistance remains a challenge.
Keywords: menin inhibitors; KMT2A rearrangements; MLL rearrangements; NPM1 mutations; acute myeloid leukemia; revumenib; precision medicine; targeted therapy

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>666</itunes:duration>
                <itunes:episode>30</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E28 - Reducing Pancreatic Surgery Complications</title>
        <itunes:title>E28 - Reducing Pancreatic Surgery Complications</itunes:title>
        <link>https://podcast.sinapsos.com/e/e28-reducing-pancreatic-surgery-complications/</link>
                    <comments>https://podcast.sinapsos.com/e/e28-reducing-pancreatic-surgery-complications/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:08:32 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/246e6cd4-b20c-3153-8c0e-0d8008b9d6bf</guid>
                                    <description><![CDATA[<p>E28   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/630'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Karpes, J.B.; Liu, K.; Crawford, M.D.; Pulitano, C.; Sandroussi, C.; Laurence, J.M. Reducing Complications in Pancreaticoduodenectomy. Cancers 2026, 18, 630. https://doi.org/10.3390/cancers18040630
Type: Review  |  Publication date: 14 February 2026

</li>
<li>Summary: Pancreatic surgery is one of the most complex areas of abdominal surgery, with morbidity and mortality remaining a major challenge. Despite progress in surgical techniques and perioperative care, outcomes still vary widely, and there is no consensus on how to reliably prevent major complications. This study evaluates contemporary evidence on how complications develop, how they can be detected early, and the strategies that may reduce their frequency and impact. The evaluation includes technical factors during surgery, as well as non-technical factors outside of the operating theatre that may improve safety and outcomes. The goal of this review is to guide practice and future research to improve the safety of pancreatic resection in any environment.

</li>
<li>Keywords: pancreaticoduodenectomy; postoperative pancreatic fistula; centralisation; failure to rescue</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E28   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/630'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Karpes, J.B.; Liu, K.; Crawford, M.D.; Pulitano, C.; Sandroussi, C.; Laurence, J.M. Reducing Complications in Pancreaticoduodenectomy. Cancers 2026, 18, 630. https://doi.org/10.3390/cancers18040630<br>
Type: Review  |  Publication date: 14 February 2026<br>
<br>
</li>
<li>Summary: Pancreatic surgery is one of the most complex areas of abdominal surgery, with morbidity and mortality remaining a major challenge. Despite progress in surgical techniques and perioperative care, outcomes still vary widely, and there is no consensus on how to reliably prevent major complications. This study evaluates contemporary evidence on how complications develop, how they can be detected early, and the strategies that may reduce their frequency and impact. The evaluation includes technical factors during surgery, as well as non-technical factors outside of the operating theatre that may improve safety and outcomes. The goal of this review is to guide practice and future research to improve the safety of pancreatic resection in any environment.<br>
<br>
</li>
<li>Keywords: pancreaticoduodenectomy; postoperative pancreatic fistula; centralisation; failure to rescue</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/5i7nz7mzbf8f69pw/E28_-_Reducing_Pancreatic_Surgery_Complications.mp3" length="17465930" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E28   |  13 min   |   Latest   |  Publication Link

Podcast based on: Karpes, J.B.; Liu, K.; Crawford, M.D.; Pulitano, C.; Sandroussi, C.; Laurence, J.M. Reducing Complications in Pancreaticoduodenectomy. Cancers 2026, 18, 630. https://doi.org/10.3390/cancers18040630Type: Review  |  Publication date: 14 February 2026
Summary: Pancreatic surgery is one of the most complex areas of abdominal surgery, with morbidity and mortality remaining a major challenge. Despite progress in surgical techniques and perioperative care, outcomes still vary widely, and there is no consensus on how to reliably prevent major complications. This study evaluates contemporary evidence on how complications develop, how they can be detected early, and the strategies that may reduce their frequency and impact. The evaluation includes technical factors during surgery, as well as non-technical factors outside of the operating theatre that may improve safety and outcomes. The goal of this review is to guide practice and future research to improve the safety of pancreatic resection in any environment.
Keywords: pancreaticoduodenectomy; postoperative pancreatic fistula; centralisation; failure to rescue

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>727</itunes:duration>
                <itunes:episode>29</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E27 - Histotripsy Boosts Survival in Brain Cancer</title>
        <itunes:title>E27 - Histotripsy Boosts Survival in Brain Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e27-histotripsy-boosts-survival-in-brain-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e27-histotripsy-boosts-survival-in-brain-cancer/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:07:46 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/f03b0017-8f55-347d-9eca-763d06ca286c</guid>
                                    <description><![CDATA[<p>E27   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/622'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Duclos, S.; Kaovasia, T.P.; Fox, A.; Cornett, A.; Pandey, A.S.; Xu, Z. First Report of Histotripsy-Induced Survival Benefit in Murine Glioblastomas. Cancers 2026, 18, 622. https://doi.org/10.3390/cancers18040622
Type: Article  |  Publication date: 13 February 2026

</li>
<li>Summary: Histotripsy is a noninvasive soft tissue ablation technique that uses high-pressure ultrasound to generate precise regions of cellular destruction within tumors while sparing surrounding healthy tissue. This study evaluated the survival benefit of a single transcranial histotripsy treatment in glioblastoma-bearing mice using a raster-scanning pattern with varying numbers of histotripsy pulses. Histotripsy resulted in an 18.5% increase in survival compared with untreated controls and was well tolerated with no significant acute or chronic adverse effects. These findings support further investigation of histotripsy as a potential therapeutic approach for brain tumors.

</li>
<li>Keywords: glioblastoma; murine model; transcranial histotripsy</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E27   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/622'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Duclos, S.; Kaovasia, T.P.; Fox, A.; Cornett, A.; Pandey, A.S.; Xu, Z. First Report of Histotripsy-Induced Survival Benefit in Murine Glioblastomas. Cancers 2026, 18, 622. https://doi.org/10.3390/cancers18040622<br>
Type: Article  |  Publication date: 13 February 2026<br>
<br>
</li>
<li>Summary: Histotripsy is a noninvasive soft tissue ablation technique that uses high-pressure ultrasound to generate precise regions of cellular destruction within tumors while sparing surrounding healthy tissue. This study evaluated the survival benefit of a single transcranial histotripsy treatment in glioblastoma-bearing mice using a raster-scanning pattern with varying numbers of histotripsy pulses. Histotripsy resulted in an 18.5% increase in survival compared with untreated controls and was well tolerated with no significant acute or chronic adverse effects. These findings support further investigation of histotripsy as a potential therapeutic approach for brain tumors.<br>
<br>
</li>
<li>Keywords: glioblastoma; murine model; transcranial histotripsy</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/2cm22t99ukeazjfd/E27_-_Histotripsy_Boosts_Survival_in_Brain_Cancer.mp3" length="16487905" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E27   |  12 min   |   Latest   |  Publication Link

Podcast based on: Duclos, S.; Kaovasia, T.P.; Fox, A.; Cornett, A.; Pandey, A.S.; Xu, Z. First Report of Histotripsy-Induced Survival Benefit in Murine Glioblastomas. Cancers 2026, 18, 622. https://doi.org/10.3390/cancers18040622Type: Article  |  Publication date: 13 February 2026
Summary: Histotripsy is a noninvasive soft tissue ablation technique that uses high-pressure ultrasound to generate precise regions of cellular destruction within tumors while sparing surrounding healthy tissue. This study evaluated the survival benefit of a single transcranial histotripsy treatment in glioblastoma-bearing mice using a raster-scanning pattern with varying numbers of histotripsy pulses. Histotripsy resulted in an 18.5% increase in survival compared with untreated controls and was well tolerated with no significant acute or chronic adverse effects. These findings support further investigation of histotripsy as a potential therapeutic approach for brain tumors.
Keywords: glioblastoma; murine model; transcranial histotripsy

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>686</itunes:duration>
                <itunes:episode>28</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E26 - Advances in Liver Cancer Treatment</title>
        <itunes:title>E26 - Advances in Liver Cancer Treatment</itunes:title>
        <link>https://podcast.sinapsos.com/e/e26-advances-in-liver-cancer-treatment/</link>
                    <comments>https://podcast.sinapsos.com/e/e26-advances-in-liver-cancer-treatment/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:07:01 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/44fd3531-2296-3c32-a34e-35bababfd949</guid>
                                    <description><![CDATA[<p>E26   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/609'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Morishita, A.; Oura, K.; Tai, H.; Yano, R.; Nakahara, M.; Tadokoro, T.; Fujita, K.; Mimura, S.; Tani, J.; Tatsuta, M.; Himoto, T.; Kobara, H. Advances in the Therapeutic Landscape of Hepatocellular Carcinoma: Current Strategies and Future Perspectives. Cancers 2026, 18, 609. https://doi.org/10.3390/cancers18040609
Type: Review  |  Publication date: 12 February 2026

</li>
<li>Summary: Hepatocellular carcinoma (HCC) arises mostly in chronically diseased livers, so clinicians must manage both an aggressive cancer and a fragile organ simultaneously. This review explains how modern HCC care has evolved into an integrated continuum: from prevention and surveillance to curative options such as resection, ablation, and transplantation, to refined locoregional therapy and immunotherapy-based systemic regimens. We highlight how treatment decisions are tailored according to tumor stage, liver function, portal hypertension, and frailty, and why preserving hepatic reserve is crucial to allow multiple lines of therapy. We also summarize emerging tools such as biomarkers, liquid biopsy, radiomics, and microbiome research that may support more precise treatment selection. Finally, we discuss special populations, safety considerations, and future strategies that combine innovative and traditional approaches to improve survival and quality of life for patients with HCC worldwide. This review aims to guide practical clinical decision-making.

</li>
<li>Keywords: hepatocellular carcinoma; cirrhosis; surveillance; Barcelona Clinic Liver Cancer; transarterial chemoembolization; radioembolization; stereotactic body radiotherapy; immune checkpoint inhibitor; tyrosine kinase inhibitor; biomarkers</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E26   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/609'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Morishita, A.; Oura, K.; Tai, H.; Yano, R.; Nakahara, M.; Tadokoro, T.; Fujita, K.; Mimura, S.; Tani, J.; Tatsuta, M.; Himoto, T.; Kobara, H. Advances in the Therapeutic Landscape of Hepatocellular Carcinoma: Current Strategies and Future Perspectives. Cancers 2026, 18, 609. https://doi.org/10.3390/cancers18040609<br>
Type: Review  |  Publication date: 12 February 2026<br>
<br>
</li>
<li>Summary: Hepatocellular carcinoma (HCC) arises mostly in chronically diseased livers, so clinicians must manage both an aggressive cancer and a fragile organ simultaneously. This review explains how modern HCC care has evolved into an integrated continuum: from prevention and surveillance to curative options such as resection, ablation, and transplantation, to refined locoregional therapy and immunotherapy-based systemic regimens. We highlight how treatment decisions are tailored according to tumor stage, liver function, portal hypertension, and frailty, and why preserving hepatic reserve is crucial to allow multiple lines of therapy. We also summarize emerging tools such as biomarkers, liquid biopsy, radiomics, and microbiome research that may support more precise treatment selection. Finally, we discuss special populations, safety considerations, and future strategies that combine innovative and traditional approaches to improve survival and quality of life for patients with HCC worldwide. This review aims to guide practical clinical decision-making.<br>
<br>
</li>
<li>Keywords: hepatocellular carcinoma; cirrhosis; surveillance; Barcelona Clinic Liver Cancer; transarterial chemoembolization; radioembolization; stereotactic body radiotherapy; immune checkpoint inhibitor; tyrosine kinase inhibitor; biomarkers</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/yhaqsvi2ehffkzgs/E26_-_Advances_in_Liver_Cancer_Treatment.mp3" length="17406371" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E26   |  13 min   |   Latest   |  Publication Link

Podcast based on: Morishita, A.; Oura, K.; Tai, H.; Yano, R.; Nakahara, M.; Tadokoro, T.; Fujita, K.; Mimura, S.; Tani, J.; Tatsuta, M.; Himoto, T.; Kobara, H. Advances in the Therapeutic Landscape of Hepatocellular Carcinoma: Current Strategies and Future Perspectives. Cancers 2026, 18, 609. https://doi.org/10.3390/cancers18040609Type: Review  |  Publication date: 12 February 2026
Summary: Hepatocellular carcinoma (HCC) arises mostly in chronically diseased livers, so clinicians must manage both an aggressive cancer and a fragile organ simultaneously. This review explains how modern HCC care has evolved into an integrated continuum: from prevention and surveillance to curative options such as resection, ablation, and transplantation, to refined locoregional therapy and immunotherapy-based systemic regimens. We highlight how treatment decisions are tailored according to tumor stage, liver function, portal hypertension, and frailty, and why preserving hepatic reserve is crucial to allow multiple lines of therapy. We also summarize emerging tools such as biomarkers, liquid biopsy, radiomics, and microbiome research that may support more precise treatment selection. Finally, we discuss special populations, safety considerations, and future strategies that combine innovative and traditional approaches to improve survival and quality of life for patients with HCC worldwide. This review aims to guide practical clinical decision-making.
Keywords: hepatocellular carcinoma; cirrhosis; surveillance; Barcelona Clinic Liver Cancer; transarterial chemoembolization; radioembolization; stereotactic body radiotherapy; immune checkpoint inhibitor; tyrosine kinase inhibitor; biomarkers

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>725</itunes:duration>
                <itunes:episode>27</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E25 - Eribulin s Effect on Breast Cancer Plasticity</title>
        <itunes:title>E25 - Eribulin s Effect on Breast Cancer Plasticity</itunes:title>
        <link>https://podcast.sinapsos.com/e/e25-eribulin-s-effect-on-breast-cancer-plasticity/</link>
                    <comments>https://podcast.sinapsos.com/e/e25-eribulin-s-effect-on-breast-cancer-plasticity/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:06:17 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/f1f8a046-3cc6-3c46-8ceb-c25c9336fb82</guid>
                                    <description><![CDATA[<p>E25   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/598'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Bidgood, C.L.; Morera, E.; Jaradi, B.; van Wyngaard, T.; Koikalethu, A.T.; Bock, N.; Agarwal, V.; Redfern, A.D.; Thompson, E.W. Effects of Eribulin on Epithelial–Mesenchymal Plasticity in Patient-Derived Breast Cancer Cultures and Excised Tissues. Cancers 2026, 18, 598. https://doi.org/10.3390/cancers18040598
Type: Article  |  Publication date: 11 February 2026

</li>
<li>Summary: Eribulin is an approved therapy for the treatment of breast cancer which has been shown to reverse the epithelial-to-mesenchymal transition (EMT) and improve the efficacy of standard chemotherapies in cell lines, animal studies, and clinical specimens. Tumour EMT status has also been linked to eribulin efficacy. Based on this, we evaluated the effects of eribulin in patient-derived breast cancer cultures and a triple-negative breast cancer cell line to assess changes to EMT and therapy response. We further identified the induction of epithelial-like characteristics, including E-cadherin expression in a patient-derived HER2+ primary tissue with a predominantly mesenchymal phenotype following longitudinal eribulin exposure. Additionally, we compared EMT marker expression in breast cancers treated with standard-of-care neoadjuvant docetaxel, Adriamycin and cyclophosphamide (TAC) therapy with that observed in the neoadjuvant eribulin clinical trial.

</li>
<li>Keywords: breast cancer; eribulin; EMT; chemoresistance</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E25   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/598'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Bidgood, C.L.; Morera, E.; Jaradi, B.; van Wyngaard, T.; Koikalethu, A.T.; Bock, N.; Agarwal, V.; Redfern, A.D.; Thompson, E.W. Effects of Eribulin on Epithelial–Mesenchymal Plasticity in Patient-Derived Breast Cancer Cultures and Excised Tissues. Cancers 2026, 18, 598. https://doi.org/10.3390/cancers18040598<br>
Type: Article  |  Publication date: 11 February 2026<br>
<br>
</li>
<li>Summary: Eribulin is an approved therapy for the treatment of breast cancer which has been shown to reverse the epithelial-to-mesenchymal transition (EMT) and improve the efficacy of standard chemotherapies in cell lines, animal studies, and clinical specimens. Tumour EMT status has also been linked to eribulin efficacy. Based on this, we evaluated the effects of eribulin in patient-derived breast cancer cultures and a triple-negative breast cancer cell line to assess changes to EMT and therapy response. We further identified the induction of epithelial-like characteristics, including E-cadherin expression in a patient-derived HER2+ primary tissue with a predominantly mesenchymal phenotype following longitudinal eribulin exposure. Additionally, we compared EMT marker expression in breast cancers treated with standard-of-care neoadjuvant docetaxel, Adriamycin and cyclophosphamide (TAC) therapy with that observed in the neoadjuvant eribulin clinical trial.<br>
<br>
</li>
<li>Keywords: breast cancer; eribulin; EMT; chemoresistance</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/xyd7xfe8kyj7x86p/E25_-_Eribulin_s_Effect_on_Breast_Cancer_Plasticity.mp3" length="16863442" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E25   |  12 min   |   Latest   |  Publication Link

Podcast based on: Bidgood, C.L.; Morera, E.; Jaradi, B.; van Wyngaard, T.; Koikalethu, A.T.; Bock, N.; Agarwal, V.; Redfern, A.D.; Thompson, E.W. Effects of Eribulin on Epithelial–Mesenchymal Plasticity in Patient-Derived Breast Cancer Cultures and Excised Tissues. Cancers 2026, 18, 598. https://doi.org/10.3390/cancers18040598Type: Article  |  Publication date: 11 February 2026
Summary: Eribulin is an approved therapy for the treatment of breast cancer which has been shown to reverse the epithelial-to-mesenchymal transition (EMT) and improve the efficacy of standard chemotherapies in cell lines, animal studies, and clinical specimens. Tumour EMT status has also been linked to eribulin efficacy. Based on this, we evaluated the effects of eribulin in patient-derived breast cancer cultures and a triple-negative breast cancer cell line to assess changes to EMT and therapy response. We further identified the induction of epithelial-like characteristics, including E-cadherin expression in a patient-derived HER2+ primary tissue with a predominantly mesenchymal phenotype following longitudinal eribulin exposure. Additionally, we compared EMT marker expression in breast cancers treated with standard-of-care neoadjuvant docetaxel, Adriamycin and cyclophosphamide (TAC) therapy with that observed in the neoadjuvant eribulin clinical trial.
Keywords: breast cancer; eribulin; EMT; chemoresistance

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>702</itunes:duration>
                <itunes:episode>26</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E24 - ABHD5 in Cancer Research Progress</title>
        <itunes:title>E24 - ABHD5 in Cancer Research Progress</itunes:title>
        <link>https://podcast.sinapsos.com/e/e24-abhd5-in-cancer-research-progress/</link>
                    <comments>https://podcast.sinapsos.com/e/e24-abhd5-in-cancer-research-progress/#comments</comments>        <pubDate>Wed, 18 Feb 2026 20:05:31 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/ec6d6202-7e4d-355f-bf03-cabd51f21d86</guid>
                                    <description><![CDATA[<p>E24   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/585'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Cai, H.; Chen, H.; Ye, J.; Jin, Z.; Huang, P. Current Research Progress on ABHD5 in Cancers. Cancers 2026, 18, 585. https://doi.org/10.3390/cancers18040585
Type: Review  |  Publication date: 10 February 2026

</li>
<li>Summary: ABHD5 is a key regulator of lipid metabolism, with context-dependent roles in cancer. It interacts with signaling pathways like AMPK/mTOR, AKT, and NF-κB, exerting either tumor-suppressive or oncogenic effects based on the tumor’s ecological and molecular context. This review synthesizes experimental and clinical evidence to clarify its multifaceted functions and explores its potential as a diagnostic marker and therapeutic target, emphasizing the need for precision strategies rather than blunt intervention.

</li>
<li>Keywords: ABHD5; lipid metabolism; cancer; pathway</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E24   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/4/585'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Cai, H.; Chen, H.; Ye, J.; Jin, Z.; Huang, P. Current Research Progress on ABHD5 in Cancers. Cancers 2026, 18, 585. https://doi.org/10.3390/cancers18040585<br>
Type: Review  |  Publication date: 10 February 2026<br>
<br>
</li>
<li>Summary: ABHD5 is a key regulator of lipid metabolism, with context-dependent roles in cancer. It interacts with signaling pathways like AMPK/mTOR, AKT, and NF-κB, exerting either tumor-suppressive or oncogenic effects based on the tumor’s ecological and molecular context. This review synthesizes experimental and clinical evidence to clarify its multifaceted functions and explores its potential as a diagnostic marker and therapeutic target, emphasizing the need for precision strategies rather than blunt intervention.<br>
<br>
</li>
<li>Keywords: ABHD5; lipid metabolism; cancer; pathway</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/rgje2uwcuyd829eq/E24_-_ABHD5_in_Cancer_Research_Progress.mp3" length="18663383" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E24   |  13 min   |   Latest   |  Publication Link

Podcast based on: Cai, H.; Chen, H.; Ye, J.; Jin, Z.; Huang, P. Current Research Progress on ABHD5 in Cancers. Cancers 2026, 18, 585. https://doi.org/10.3390/cancers18040585Type: Review  |  Publication date: 10 February 2026
Summary: ABHD5 is a key regulator of lipid metabolism, with context-dependent roles in cancer. It interacts with signaling pathways like AMPK/mTOR, AKT, and NF-κB, exerting either tumor-suppressive or oncogenic effects based on the tumor’s ecological and molecular context. This review synthesizes experimental and clinical evidence to clarify its multifaceted functions and explores its potential as a diagnostic marker and therapeutic target, emphasizing the need for precision strategies rather than blunt intervention.
Keywords: ABHD5; lipid metabolism; cancer; pathway

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>777</itunes:duration>
                <itunes:episode>25</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
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    <item>
        <title>E23 - Surgery for Mediastinal Paragangliomas 20-Year Review</title>
        <itunes:title>E23 - Surgery for Mediastinal Paragangliomas 20-Year Review</itunes:title>
        <link>https://podcast.sinapsos.com/e/e23-surgery-for-mediastinal-paragangliomas-20-year-review/</link>
                    <comments>https://podcast.sinapsos.com/e/e23-surgery-for-mediastinal-paragangliomas-20-year-review/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:13:38 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/a49ce846-38f5-3d23-8a9d-d13bc4345dd5</guid>
                                    <description><![CDATA[<p>E23   |  16 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/486'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Rotolo, N.; Cerretani, G.; Casagrande, S.; Nardecchia, E.; Asteggiano, E.; Colombo, A.; Filipponi, L.; Piacentino, F.; Ilaria, S.; Fontana, F. Surgical Approaches and Perioperative Outcomes in Mediastinal Paragangliomas: A 20-Year Comprehensive Systematic Review. Cancers 2026, 18, 486. https://doi.org/10.3390/cancers18030486
Type: Systematic Review  |  Publication date: 01 February 2026

</li>
<li>Summary: This study reviews the surgical management of a mediastinal paraganglioma, a rare type of tumor that is often located in the posterior mediastinum and can surround or involve the heart and major blood vessels. Often asymptomatic or with symptoms related to catecholamine secretion, the surgical approach is the treatment of choice, achieving local disease control and long-term outcomes. However, surgical removal poses a high risk of severe bleeding and perioperative complications. By analyzing literature from the last twenty years, we aim to establish a clearer and safer approach for diagnosis and surgery. The findings will help surgeons better plan these complex operations, potentially reducing complications and improving patient care for this uncommon but dangerous condition.

</li>
<li>Keywords: mediastinal paraganglioma; surgical resection; cardiopulmonary by-pass; post-operative complications; systematic review</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E23   |  16 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/486'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Rotolo, N.; Cerretani, G.; Casagrande, S.; Nardecchia, E.; Asteggiano, E.; Colombo, A.; Filipponi, L.; Piacentino, F.; Ilaria, S.; Fontana, F. Surgical Approaches and Perioperative Outcomes in Mediastinal Paragangliomas: A 20-Year Comprehensive Systematic Review. Cancers 2026, 18, 486. https://doi.org/10.3390/cancers18030486<br>
Type: Systematic Review  |  Publication date: 01 February 2026<br>
<br>
</li>
<li>Summary: This study reviews the surgical management of a mediastinal paraganglioma, a rare type of tumor that is often located in the posterior mediastinum and can surround or involve the heart and major blood vessels. Often asymptomatic or with symptoms related to catecholamine secretion, the surgical approach is the treatment of choice, achieving local disease control and long-term outcomes. However, surgical removal poses a high risk of severe bleeding and perioperative complications. By analyzing literature from the last twenty years, we aim to establish a clearer and safer approach for diagnosis and surgery. The findings will help surgeons better plan these complex operations, potentially reducing complications and improving patient care for this uncommon but dangerous condition.<br>
<br>
</li>
<li>Keywords: mediastinal paraganglioma; surgical resection; cardiopulmonary by-pass; post-operative complications; systematic review</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/4p8g9nze5rig5hqk/E23_-_Surgery_for_Mediastinal_Paragangliomas_20-Year_Review.mp3" length="22218126" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E23   |  16 min   |   Latest   |  Publication Link

Podcast based on: Rotolo, N.; Cerretani, G.; Casagrande, S.; Nardecchia, E.; Asteggiano, E.; Colombo, A.; Filipponi, L.; Piacentino, F.; Ilaria, S.; Fontana, F. Surgical Approaches and Perioperative Outcomes in Mediastinal Paragangliomas: A 20-Year Comprehensive Systematic Review. Cancers 2026, 18, 486. https://doi.org/10.3390/cancers18030486Type: Systematic Review  |  Publication date: 01 February 2026
Summary: This study reviews the surgical management of a mediastinal paraganglioma, a rare type of tumor that is often located in the posterior mediastinum and can surround or involve the heart and major blood vessels. Often asymptomatic or with symptoms related to catecholamine secretion, the surgical approach is the treatment of choice, achieving local disease control and long-term outcomes. However, surgical removal poses a high risk of severe bleeding and perioperative complications. By analyzing literature from the last twenty years, we aim to establish a clearer and safer approach for diagnosis and surgery. The findings will help surgeons better plan these complex operations, potentially reducing complications and improving patient care for this uncommon but dangerous condition.
Keywords: mediastinal paraganglioma; surgical resection; cardiopulmonary by-pass; post-operative complications; systematic review

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>925</itunes:duration>
                <itunes:episode>24</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E22 - SLPI s Role in Prostate Cancer</title>
        <itunes:title>E22 - SLPI s Role in Prostate Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e22-slpi-s-role-in-prostate-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e22-slpi-s-role-in-prostate-cancer/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:12:52 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/1c56d6b5-593e-38a7-8926-36b3f3a4f081</guid>
                                    <description><![CDATA[<p>E22   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/487'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Rosini, D.; Cosi, I.; De Iaco, P.; Sebastianelli, A.; Di Stefano, G.; Serni, S.; Nesi, G.; Notaro, R.; De Angioletti, M. SLPI in Prostate Cancer. Cancers 2026, 18, 487. https://doi.org/10.3390/cancers18030487
Type: Review  |  Publication date: 01 February 2026

</li>
<li>Summary: SLPI is a protein that usually acts as a protective shield for our body’s internal surfaces. Its main jobs are to prevent tissue damage, fight germs, and control inflammation. However, in the context of cancer, SLPI acts like a double-edged sword. While it normally keeps us healthy, many cancers—including lung and breast cancer—hijack this protein to grow and spread more easily. In these cases, high levels of SLPI often signal a more aggressive disease. Interestingly, the opposite happens in some cases, like liver cancer, where more SLPI can be a positive sign. Prostate cancer shows a unique pattern: SLPI protein levels are low in the early stages but rise sharply as the cancer becomes advanced and resistant to treatments. By studying these shifts, scientists can better understand how a tumor behaves, helping doctors predict the disease’s path and develop more effective, personalized treatments for patients.

</li>
<li>Keywords: androgen; androgen receptor; biomarker; ETS transcription factors; ETV1; ETV4; transgenic mouse model; prostate cancer; secretory leukocyte protease inhibitor; SLPI</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E22   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/487'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Rosini, D.; Cosi, I.; De Iaco, P.; Sebastianelli, A.; Di Stefano, G.; Serni, S.; Nesi, G.; Notaro, R.; De Angioletti, M. SLPI in Prostate Cancer. Cancers 2026, 18, 487. https://doi.org/10.3390/cancers18030487<br>
Type: Review  |  Publication date: 01 February 2026<br>
<br>
</li>
<li>Summary: SLPI is a protein that usually acts as a protective shield for our body’s internal surfaces. Its main jobs are to prevent tissue damage, fight germs, and control inflammation. However, in the context of cancer, SLPI acts like a double-edged sword. While it normally keeps us healthy, many cancers—including lung and breast cancer—hijack this protein to grow and spread more easily. In these cases, high levels of SLPI often signal a more aggressive disease. Interestingly, the opposite happens in some cases, like liver cancer, where more SLPI can be a positive sign. Prostate cancer shows a unique pattern: SLPI protein levels are low in the early stages but rise sharply as the cancer becomes advanced and resistant to treatments. By studying these shifts, scientists can better understand how a tumor behaves, helping doctors predict the disease’s path and develop more effective, personalized treatments for patients.<br>
<br>
</li>
<li>Keywords: androgen; androgen receptor; biomarker; ETS transcription factors; ETV1; ETV4; transgenic mouse model; prostate cancer; secretory leukocyte protease inhibitor; SLPI</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/jek6bbavv4v7g4ed/E22_-_SLPI_s_Role_in_Prostate_Cancer.mp3" length="15558782" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E22   |  11 min   |   Latest   |  Publication Link

Podcast based on: Rosini, D.; Cosi, I.; De Iaco, P.; Sebastianelli, A.; Di Stefano, G.; Serni, S.; Nesi, G.; Notaro, R.; De Angioletti, M. SLPI in Prostate Cancer. Cancers 2026, 18, 487. https://doi.org/10.3390/cancers18030487Type: Review  |  Publication date: 01 February 2026
Summary: SLPI is a protein that usually acts as a protective shield for our body’s internal surfaces. Its main jobs are to prevent tissue damage, fight germs, and control inflammation. However, in the context of cancer, SLPI acts like a double-edged sword. While it normally keeps us healthy, many cancers—including lung and breast cancer—hijack this protein to grow and spread more easily. In these cases, high levels of SLPI often signal a more aggressive disease. Interestingly, the opposite happens in some cases, like liver cancer, where more SLPI can be a positive sign. Prostate cancer shows a unique pattern: SLPI protein levels are low in the early stages but rise sharply as the cancer becomes advanced and resistant to treatments. By studying these shifts, scientists can better understand how a tumor behaves, helping doctors predict the disease’s path and develop more effective, personalized treatments for patients.
Keywords: androgen; androgen receptor; biomarker; ETS transcription factors; ETV1; ETV4; transgenic mouse model; prostate cancer; secretory leukocyte protease inhibitor; SLPI

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>648</itunes:duration>
                <itunes:episode>23</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E21 - PBK Expression and Immune-Activated Colorectal Cancer</title>
        <itunes:title>E21 - PBK Expression and Immune-Activated Colorectal Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e21-pbk-expression-and-immune-activated-colorectal-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e21-pbk-expression-and-immune-activated-colorectal-cancer/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:12:07 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/50c5a323-789b-3403-b813-bc41f9a87771</guid>
                                    <description><![CDATA[<p>E21   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/482'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Sawaguchi, H.; Uehara, T.; Iwaya, M.; Asaka, S.; Nakajima, T.; Komamura, S.; Imamura, S.; Iwaya, Y.; Sugenoya, S.; Kitazawa, M.; Soejima, Y.; Ota, H.; Nagaya, T. The Correlation of PBK Expression with an Immune-Activated Tumor Microenvironment and Outcome in Colorectal Cancer. Cancers 2026, 18, 482. https://doi.org/10.3390/cancers18030482
Type: Article  |  Publication date: 31 January 2026

</li>
<li>Summary: Colorectal cancer shows large differences in patient outcomes, partly because tumors vary in their biological and immune characteristics. Identifying markers that reflect these differences is important for improving prognosis and treatment strategies. PDZ-binding kinase (PBK) is a protein involved in cell division and has been linked to cancer progression, but its clinical significance in colorectal cancer remains unclear. In this study, we examined PBK expression in tumor tissues from patients with colorectal cancer and analyzed its relationship with tumor features, immune cell infiltration, and patient survival. We found that tumors with high PBK expression were associated with a more active immune environment and better clinical outcomes. These findings suggest that PBK expression may help identify colorectal cancer patients with a favorable immune response and prognosis, providing useful information for future research and potential treatment stratification.

</li>
<li>Keywords: colorectal cancer; tumor microenvironment; prognosis; immune microenvironment</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E21   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/482'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Sawaguchi, H.; Uehara, T.; Iwaya, M.; Asaka, S.; Nakajima, T.; Komamura, S.; Imamura, S.; Iwaya, Y.; Sugenoya, S.; Kitazawa, M.; Soejima, Y.; Ota, H.; Nagaya, T. The Correlation of PBK Expression with an Immune-Activated Tumor Microenvironment and Outcome in Colorectal Cancer. Cancers 2026, 18, 482. https://doi.org/10.3390/cancers18030482<br>
Type: Article  |  Publication date: 31 January 2026<br>
<br>
</li>
<li>Summary: Colorectal cancer shows large differences in patient outcomes, partly because tumors vary in their biological and immune characteristics. Identifying markers that reflect these differences is important for improving prognosis and treatment strategies. PDZ-binding kinase (PBK) is a protein involved in cell division and has been linked to cancer progression, but its clinical significance in colorectal cancer remains unclear. In this study, we examined PBK expression in tumor tissues from patients with colorectal cancer and analyzed its relationship with tumor features, immune cell infiltration, and patient survival. We found that tumors with high PBK expression were associated with a more active immune environment and better clinical outcomes. These findings suggest that PBK expression may help identify colorectal cancer patients with a favorable immune response and prognosis, providing useful information for future research and potential treatment stratification.<br>
<br>
</li>
<li>Keywords: colorectal cancer; tumor microenvironment; prognosis; immune microenvironment</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/ht7uukq4xvhf793i/E21_-_PBK_Expression_and_Immune-Activated_Colorectal_Cancer.mp3" length="17225812" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E21   |  12 min   |   Latest   |  Publication Link

Podcast based on: Sawaguchi, H.; Uehara, T.; Iwaya, M.; Asaka, S.; Nakajima, T.; Komamura, S.; Imamura, S.; Iwaya, Y.; Sugenoya, S.; Kitazawa, M.; Soejima, Y.; Ota, H.; Nagaya, T. The Correlation of PBK Expression with an Immune-Activated Tumor Microenvironment and Outcome in Colorectal Cancer. Cancers 2026, 18, 482. https://doi.org/10.3390/cancers18030482Type: Article  |  Publication date: 31 January 2026
Summary: Colorectal cancer shows large differences in patient outcomes, partly because tumors vary in their biological and immune characteristics. Identifying markers that reflect these differences is important for improving prognosis and treatment strategies. PDZ-binding kinase (PBK) is a protein involved in cell division and has been linked to cancer progression, but its clinical significance in colorectal cancer remains unclear. In this study, we examined PBK expression in tumor tissues from patients with colorectal cancer and analyzed its relationship with tumor features, immune cell infiltration, and patient survival. We found that tumors with high PBK expression were associated with a more active immune environment and better clinical outcomes. These findings suggest that PBK expression may help identify colorectal cancer patients with a favorable immune response and prognosis, providing useful information for future research and potential treatment stratification.
Keywords: colorectal cancer; tumor microenvironment; prognosis; immune microenvironment

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>717</itunes:duration>
                <itunes:episode>22</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E20 - Multi-Targeted TKIs for Advanced Ewing Sarcoma</title>
        <itunes:title>E20 - Multi-Targeted TKIs for Advanced Ewing Sarcoma</itunes:title>
        <link>https://podcast.sinapsos.com/e/e20-multi-targeted-tkis-for-advanced-ewing-sarcoma/</link>
                    <comments>https://podcast.sinapsos.com/e/e20-multi-targeted-tkis-for-advanced-ewing-sarcoma/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:11:21 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/2dc41268-724a-31d6-b802-aa41df70a501</guid>
                                    <description><![CDATA[<p>E20   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/465'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Michelon, I.; do Rêgo Castro, C.E.; Querino Belluco, A.P.; Dacoregio, M.I.; Priantti, J.; Witt, R.G.; Attia, S.; Vilbert, M.; Cavalcante, L. Multi-Targeted TKIs in Patients with Advanced Ewing Sarcoma: A Systematic Review and Single-Arm Meta-Analysis. Cancers 2026, 18, 465. https://doi.org/10.3390/cancers18030465
Type: Systematic Review  |  Publication date: 30 January 2026

</li>
<li>Summary: Ewing sarcoma is a rare and aggressive cancer that often relapses after treatment. There is no clear standard therapy for patients whose disease progresses. Tyrosine kinase inhibitors have recently shown promising results. We reviewed and pooled data from published clinical trials and real-world studies to better evaluate the efficacy and safety of tyrosine kinase inhibitors in relapsed Ewing sarcoma patients. In our pooled analyses of 14 studies, we found an objective response rate of 23% and a disease control rate of 61.1%. Cabozantinib and regorafenib showed the most consistent benefits among drugs available in Western countries. These findings suggest the potential of tyrosine kinase inhibitors in the treatment of such a challenging population.

</li>
<li>Keywords: tyrosine kinase inhibitor; Ewing sarcoma; multiply refractory disease; TKI</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E20   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/465'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Michelon, I.; do Rêgo Castro, C.E.; Querino Belluco, A.P.; Dacoregio, M.I.; Priantti, J.; Witt, R.G.; Attia, S.; Vilbert, M.; Cavalcante, L. Multi-Targeted TKIs in Patients with Advanced Ewing Sarcoma: A Systematic Review and Single-Arm Meta-Analysis. Cancers 2026, 18, 465. https://doi.org/10.3390/cancers18030465<br>
Type: Systematic Review  |  Publication date: 30 January 2026<br>
<br>
</li>
<li>Summary: Ewing sarcoma is a rare and aggressive cancer that often relapses after treatment. There is no clear standard therapy for patients whose disease progresses. Tyrosine kinase inhibitors have recently shown promising results. We reviewed and pooled data from published clinical trials and real-world studies to better evaluate the efficacy and safety of tyrosine kinase inhibitors in relapsed Ewing sarcoma patients. In our pooled analyses of 14 studies, we found an objective response rate of 23% and a disease control rate of 61.1%. Cabozantinib and regorafenib showed the most consistent benefits among drugs available in Western countries. These findings suggest the potential of tyrosine kinase inhibitors in the treatment of such a challenging population.<br>
<br>
</li>
<li>Keywords: tyrosine kinase inhibitor; Ewing sarcoma; multiply refractory disease; TKI</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/ryifqbti22pe395e/E20_-_Multi-Targeted_TKIs_for_Advanced_Ewing_Sarcoma.mp3" length="15523047" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E20   |  11 min   |   Latest   |  Publication Link

Podcast based on: Michelon, I.; do Rêgo Castro, C.E.; Querino Belluco, A.P.; Dacoregio, M.I.; Priantti, J.; Witt, R.G.; Attia, S.; Vilbert, M.; Cavalcante, L. Multi-Targeted TKIs in Patients with Advanced Ewing Sarcoma: A Systematic Review and Single-Arm Meta-Analysis. Cancers 2026, 18, 465. https://doi.org/10.3390/cancers18030465Type: Systematic Review  |  Publication date: 30 January 2026
Summary: Ewing sarcoma is a rare and aggressive cancer that often relapses after treatment. There is no clear standard therapy for patients whose disease progresses. Tyrosine kinase inhibitors have recently shown promising results. We reviewed and pooled data from published clinical trials and real-world studies to better evaluate the efficacy and safety of tyrosine kinase inhibitors in relapsed Ewing sarcoma patients. In our pooled analyses of 14 studies, we found an objective response rate of 23% and a disease control rate of 61.1%. Cabozantinib and regorafenib showed the most consistent benefits among drugs available in Western countries. These findings suggest the potential of tyrosine kinase inhibitors in the treatment of such a challenging population.
Keywords: tyrosine kinase inhibitor; Ewing sarcoma; multiply refractory disease; TKI

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>646</itunes:duration>
                <itunes:episode>21</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E19 - Endometrial Mixed Carcinomas Clinicopathologic Insights</title>
        <itunes:title>E19 - Endometrial Mixed Carcinomas Clinicopathologic Insights</itunes:title>
        <link>https://podcast.sinapsos.com/e/e19-endometrial-mixed-carcinomas-clinicopathologic-insights/</link>
                    <comments>https://podcast.sinapsos.com/e/e19-endometrial-mixed-carcinomas-clinicopathologic-insights/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:10:36 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/cac4fa5d-ea0a-3354-916b-92fe63573175</guid>
                                    <description><![CDATA[<p>E19   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/440'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Bhardwaj, S.; Saleh, M.; Kinoshita, Y.; Brody, R.; Lukatskaya, O.; Blank, S.V.; Baskovich, B.; Kalir, T. Endometrial Mixed and Mixed-Feature Carcinomas: Small Cohort Clinicopathologic and Molecular Studies. Cancers 2026, 18, 440. https://doi.org/10.3390/cancers18030440
Type: Article  |  Publication date: 29 January 2026

</li>
<li>Summary: Endometrial cancer is a prevalent disease worldwide. There are different kinds of endometrial cancers and their treatment is based on the specific type of cancer—termed the histologic type, and the extent of disease spread—termed stage. The pathology diagnosis of the specific type of endometrial cancer is improving because of our ability to identify specific gene mutations that are unique to the different histologic groups of endometrial cancer. Discovering more about these gene mutations will enable us to design better, more personalized treatment, and avoid having patients try medicines that may not be effective at eliminating their tumor cells. In this current research investigation, we studied a rare sub group of endometrial cancers called mixed carcinomas. There are currently no treatment guidelines for this particular group, and we wanted to learn more about their gene mutations in order to better guide future therapy.

</li>
<li>Keywords: mixed endometrial cancer; mixed-feature endometrial cancer; molecular genetics; endometrial cancer</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E19   |  13 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/440'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Bhardwaj, S.; Saleh, M.; Kinoshita, Y.; Brody, R.; Lukatskaya, O.; Blank, S.V.; Baskovich, B.; Kalir, T. Endometrial Mixed and Mixed-Feature Carcinomas: Small Cohort Clinicopathologic and Molecular Studies. Cancers 2026, 18, 440. https://doi.org/10.3390/cancers18030440<br>
Type: Article  |  Publication date: 29 January 2026<br>
<br>
</li>
<li>Summary: Endometrial cancer is a prevalent disease worldwide. There are different kinds of endometrial cancers and their treatment is based on the specific type of cancer—termed the histologic type, and the extent of disease spread—termed stage. The pathology diagnosis of the specific type of endometrial cancer is improving because of our ability to identify specific gene mutations that are unique to the different histologic groups of endometrial cancer. Discovering more about these gene mutations will enable us to design better, more personalized treatment, and avoid having patients try medicines that may not be effective at eliminating their tumor cells. In this current research investigation, we studied a rare sub group of endometrial cancers called mixed carcinomas. There are currently no treatment guidelines for this particular group, and we wanted to learn more about their gene mutations in order to better guide future therapy.<br>
<br>
</li>
<li>Keywords: mixed endometrial cancer; mixed-feature endometrial cancer; molecular genetics; endometrial cancer</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/tg9nivnz6iffgt8f/E19_-_Endometrial_Mixed_Carcinomas_Clinicopathologic_Insights.mp3" length="17319853" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E19   |  13 min   |   Latest   |  Publication Link

Podcast based on: Bhardwaj, S.; Saleh, M.; Kinoshita, Y.; Brody, R.; Lukatskaya, O.; Blank, S.V.; Baskovich, B.; Kalir, T. Endometrial Mixed and Mixed-Feature Carcinomas: Small Cohort Clinicopathologic and Molecular Studies. Cancers 2026, 18, 440. https://doi.org/10.3390/cancers18030440Type: Article  |  Publication date: 29 January 2026
Summary: Endometrial cancer is a prevalent disease worldwide. There are different kinds of endometrial cancers and their treatment is based on the specific type of cancer—termed the histologic type, and the extent of disease spread—termed stage. The pathology diagnosis of the specific type of endometrial cancer is improving because of our ability to identify specific gene mutations that are unique to the different histologic groups of endometrial cancer. Discovering more about these gene mutations will enable us to design better, more personalized treatment, and avoid having patients try medicines that may not be effective at eliminating their tumor cells. In this current research investigation, we studied a rare sub group of endometrial cancers called mixed carcinomas. There are currently no treatment guidelines for this particular group, and we wanted to learn more about their gene mutations in order to better guide future therapy.
Keywords: mixed endometrial cancer; mixed-feature endometrial cancer; molecular genetics; endometrial cancer

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>721</itunes:duration>
                <itunes:episode>20</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E18 - Multi-Target Radiotherapy Conformity Index</title>
        <itunes:title>E18 - Multi-Target Radiotherapy Conformity Index</itunes:title>
        <link>https://podcast.sinapsos.com/e/e18-multi-target-radiotherapy-conformity-index/</link>
                    <comments>https://podcast.sinapsos.com/e/e18-multi-target-radiotherapy-conformity-index/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:09:50 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/b619867f-29e7-3950-9ea3-08cc5a383e5b</guid>
                                    <description><![CDATA[<p>E18   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/426'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Sang, Y.; Dang, J.; Wu, J.; Wu, Y.; Quan, E.; Dai, J. Generalization of the Conformity Index for Multi-Target Radiotherapy Plans. Cancers 2026, 18, 426. https://doi.org/10.3390/cancers18030426
Type: Article  |  Publication date: 28 January 2026

</li>
<li>Summary: This study proposes a generalized method to calculate the Conformity Index (CI) for multi-target radiotherapy plans (e.g., breast or nasopharyngeal cancer). Standard CI formulas are often distorted in these complex scenarios because they erroneously include dose spillover from adjacent targets. To address this, we redefined the Target Volume (VTV) parameter to mathematically isolate the prescription dose region of each specific target. Validation on clinical plans demonstrated that the new formula effectively eliminates interference from neighboring targets, providing CI values that accurately reflect the true dose conformity. This improved calculation is recommended for the objective evaluation of multi-target radiotherapy plans.

</li>
<li>Keywords: radiotherapy planning; generalized conformity index; evaluation; multi-target plans</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E18   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/426'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Sang, Y.; Dang, J.; Wu, J.; Wu, Y.; Quan, E.; Dai, J. Generalization of the Conformity Index for Multi-Target Radiotherapy Plans. Cancers 2026, 18, 426. https://doi.org/10.3390/cancers18030426<br>
Type: Article  |  Publication date: 28 January 2026<br>
<br>
</li>
<li>Summary: This study proposes a generalized method to calculate the Conformity Index (CI) for multi-target radiotherapy plans (e.g., breast or nasopharyngeal cancer). Standard CI formulas are often distorted in these complex scenarios because they erroneously include dose spillover from adjacent targets. To address this, we redefined the Target Volume (VTV) parameter to mathematically isolate the prescription dose region of each specific target. Validation on clinical plans demonstrated that the new formula effectively eliminates interference from neighboring targets, providing CI values that accurately reflect the true dose conformity. This improved calculation is recommended for the objective evaluation of multi-target radiotherapy plans.<br>
<br>
</li>
<li>Keywords: radiotherapy planning; generalized conformity index; evaluation; multi-target plans</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/rk2f4k8entichzua/E18_-_Multi-Target_Radiotherapy_Conformity_Index.mp3" length="15860967" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E18   |  12 min   |   Latest   |  Publication Link

Podcast based on: Sang, Y.; Dang, J.; Wu, J.; Wu, Y.; Quan, E.; Dai, J. Generalization of the Conformity Index for Multi-Target Radiotherapy Plans. Cancers 2026, 18, 426. https://doi.org/10.3390/cancers18030426Type: Article  |  Publication date: 28 January 2026
Summary: This study proposes a generalized method to calculate the Conformity Index (CI) for multi-target radiotherapy plans (e.g., breast or nasopharyngeal cancer). Standard CI formulas are often distorted in these complex scenarios because they erroneously include dose spillover from adjacent targets. To address this, we redefined the Target Volume (VTV) parameter to mathematically isolate the prescription dose region of each specific target. Validation on clinical plans demonstrated that the new formula effectively eliminates interference from neighboring targets, providing CI values that accurately reflect the true dose conformity. This improved calculation is recommended for the objective evaluation of multi-target radiotherapy plans.
Keywords: radiotherapy planning; generalized conformity index; evaluation; multi-target plans

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>660</itunes:duration>
                <itunes:episode>19</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E17 - Fragmented Care Doubles Sarcoma Recurrence Risk</title>
        <itunes:title>E17 - Fragmented Care Doubles Sarcoma Recurrence Risk</itunes:title>
        <link>https://podcast.sinapsos.com/e/e17-fragmented-care-doubles-sarcoma-recurrence-risk/</link>
                    <comments>https://podcast.sinapsos.com/e/e17-fragmented-care-doubles-sarcoma-recurrence-risk/#comments</comments>        <pubDate>Mon, 02 Feb 2026 01:09:04 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/70abcef4-b785-3eaf-ad9d-698acc7cc327</guid>
                                    <description><![CDATA[<p>E17   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/387'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Schärer, M.; Heesen, P.; Studer, G.; Vogel, B.; Fuchs, B. Organizing Care Matters: Fragmented Pathways Double Early Local Recurrence Risk in Sarcoma. Cancers 2026, 18, 387. https://doi.org/10.3390/cancers18030387
Type: Article  |  Publication date: 27 January 2026

</li>
<li>Summary: Sarcomas are rare malignancies in which outcomes strongly depend on early management according to established guidelines in specialized centers. Nevertheless, many patients receive initial treatment outside structured sarcoma care pathways, where diagnostic and surgical standards are often not fully met. In this study, we analyzed patients with local recurrence within the Swiss Sarcoma Network to assess how the initial care pathway influences the risk of early recurrence. We found that fragmented initial management was independently associated with a higher risk of early local recurrence, mainly due to unplanned surgery and incomplete tumor removal. This increased risk was not compensated for by adjuvant treatments. Our findings highlight the importance of early referral and coordinated, center-based care to improve outcomes in patients with musculoskeletal sarcoma.

</li>
<li>Keywords: sarcoma; local recurrence; care pathway; fragmented care; unplanned “whoops” excision; surgical margins; multidisciplinary care; real-world data</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E17   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/3/387'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Schärer, M.; Heesen, P.; Studer, G.; Vogel, B.; Fuchs, B. Organizing Care Matters: Fragmented Pathways Double Early Local Recurrence Risk in Sarcoma. Cancers 2026, 18, 387. https://doi.org/10.3390/cancers18030387<br>
Type: Article  |  Publication date: 27 January 2026<br>
<br>
</li>
<li>Summary: Sarcomas are rare malignancies in which outcomes strongly depend on early management according to established guidelines in specialized centers. Nevertheless, many patients receive initial treatment outside structured sarcoma care pathways, where diagnostic and surgical standards are often not fully met. In this study, we analyzed patients with local recurrence within the Swiss Sarcoma Network to assess how the initial care pathway influences the risk of early recurrence. We found that fragmented initial management was independently associated with a higher risk of early local recurrence, mainly due to unplanned surgery and incomplete tumor removal. This increased risk was not compensated for by adjuvant treatments. Our findings highlight the importance of early referral and coordinated, center-based care to improve outcomes in patients with musculoskeletal sarcoma.<br>
<br>
</li>
<li>Keywords: sarcoma; local recurrence; care pathway; fragmented care; unplanned “whoops” excision; surgical margins; multidisciplinary care; real-world data</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/4ddg2823efshabu2/E17_-_Fragmented_Care_Doubles_Sarcoma_Recurrence_Risk.mp3" length="13043504" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E17   |  10 min   |   Latest   |  Publication Link

Podcast based on: Schärer, M.; Heesen, P.; Studer, G.; Vogel, B.; Fuchs, B. Organizing Care Matters: Fragmented Pathways Double Early Local Recurrence Risk in Sarcoma. Cancers 2026, 18, 387. https://doi.org/10.3390/cancers18030387Type: Article  |  Publication date: 27 January 2026
Summary: Sarcomas are rare malignancies in which outcomes strongly depend on early management according to established guidelines in specialized centers. Nevertheless, many patients receive initial treatment outside structured sarcoma care pathways, where diagnostic and surgical standards are often not fully met. In this study, we analyzed patients with local recurrence within the Swiss Sarcoma Network to assess how the initial care pathway influences the risk of early recurrence. We found that fragmented initial management was independently associated with a higher risk of early local recurrence, mainly due to unplanned surgery and incomplete tumor removal. This increased risk was not compensated for by adjuvant treatments. Our findings highlight the importance of early referral and coordinated, center-based care to improve outcomes in patients with musculoskeletal sarcoma.
Keywords: sarcoma; local recurrence; care pathway; fragmented care; unplanned “whoops” excision; surgical margins; multidisciplinary care; real-world data

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>543</itunes:duration>
                <itunes:episode>18</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E16 - Prostate Cancer Surveillance</title>
        <itunes:title>E16 - Prostate Cancer Surveillance</itunes:title>
        <link>https://podcast.sinapsos.com/e/e16-prostate-cancer-surveillance-v1/</link>
                    <comments>https://podcast.sinapsos.com/e/e16-prostate-cancer-surveillance-v1/#comments</comments>        <pubDate>Tue, 20 Jan 2026 22:20:39 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/0fc3fe97-8216-337f-a215-83434ac65fa2</guid>
                                    <description><![CDATA[<p>E16   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/292'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Sandhu, K.; Lophatananon, A.; Gnanapragasam, V.J. The Impact of Endpoint Definitions on Predictors of Progression in Active Surveillance for Early Prostate Cancer. Cancers 2026, 18, 292. https://doi.org/10.3390/cancers18020292
Type: Article  |  Publication date: 17 January 2026

</li>
<li>Summary: Active surveillance (AS) is a critically important management strategy for men with favourable-prognosis prostate cancer. However, there is no standardised or internationally agreed-upon definition of a disease progression endpoint for when AS should stop. This has led to uncertainty regarding which baseline variables reliably predict progression. In the literature, there has also been a multitude of proposed biopsy and imaging metrics that are purported to predict AS progression. We utilised the STRATified CANcer Surveillance (STRATCANs) prospective AS database to assess the utility of different clinicopathological variables in predicting progression and against different contemporary AS endpoint definitions. In this study, we found that the AS endpoint definition appears to determine which variables predict progression. Neither the addition of biopsy nor imaging metrics added consistent incremental value in better predicting progression events. PSA density, in contrast, consistently predicted progression events across different endpoint definitions.

</li>
<li>Keywords: prostate cancer; active surveillance; STRATCANs; Cambridge prognostic group</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E16   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/292'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Sandhu, K.; Lophatananon, A.; Gnanapragasam, V.J. The Impact of Endpoint Definitions on Predictors of Progression in Active Surveillance for Early Prostate Cancer. Cancers 2026, 18, 292. https://doi.org/10.3390/cancers18020292<br>
Type: Article  |  Publication date: 17 January 2026<br>
<br>
</li>
<li>Summary: Active surveillance (AS) is a critically important management strategy for men with favourable-prognosis prostate cancer. However, there is no standardised or internationally agreed-upon definition of a disease progression endpoint for when AS should stop. This has led to uncertainty regarding which baseline variables reliably predict progression. In the literature, there has also been a multitude of proposed biopsy and imaging metrics that are purported to predict AS progression. We utilised the STRATified CANcer Surveillance (STRATCANs) prospective AS database to assess the utility of different clinicopathological variables in predicting progression and against different contemporary AS endpoint definitions. In this study, we found that the AS endpoint definition appears to determine which variables predict progression. Neither the addition of biopsy nor imaging metrics added consistent incremental value in better predicting progression events. PSA density, in contrast, consistently predicted progression events across different endpoint definitions.<br>
<br>
</li>
<li>Keywords: prostate cancer; active surveillance; STRATCANs; Cambridge prognostic group</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/2g5inv9asty845gb/E16_-_Prostate_Cancer_Surveillance.mp3" length="17214528" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E16   |  12 min   |   Latest   |  Publication Link

Podcast based on: Sandhu, K.; Lophatananon, A.; Gnanapragasam, V.J. The Impact of Endpoint Definitions on Predictors of Progression in Active Surveillance for Early Prostate Cancer. Cancers 2026, 18, 292. https://doi.org/10.3390/cancers18020292Type: Article  |  Publication date: 17 January 2026
Summary: Active surveillance (AS) is a critically important management strategy for men with favourable-prognosis prostate cancer. However, there is no standardised or internationally agreed-upon definition of a disease progression endpoint for when AS should stop. This has led to uncertainty regarding which baseline variables reliably predict progression. In the literature, there has also been a multitude of proposed biopsy and imaging metrics that are purported to predict AS progression. We utilised the STRATified CANcer Surveillance (STRATCANs) prospective AS database to assess the utility of different clinicopathological variables in predicting progression and against different contemporary AS endpoint definitions. In this study, we found that the AS endpoint definition appears to determine which variables predict progression. Neither the addition of biopsy nor imaging metrics added consistent incremental value in better predicting progression events. PSA density, in contrast, consistently predicted progression events across different endpoint definitions.
Keywords: prostate cancer; active surveillance; STRATCANs; Cambridge prognostic group

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>717</itunes:duration>
                <itunes:episode>17</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E15 - Prehabilitation in Cancer Care</title>
        <itunes:title>E15 - Prehabilitation in Cancer Care</itunes:title>
        <link>https://podcast.sinapsos.com/e/e15-prehabilitation-in-cancer-care/</link>
                    <comments>https://podcast.sinapsos.com/e/e15-prehabilitation-in-cancer-care/#comments</comments>        <pubDate>Sun, 18 Jan 2026 20:43:34 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/aee0e13f-93d1-3d19-b87a-02eedd0adc52</guid>
                                    <description><![CDATA[<p>E15   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/286'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Kwan, D.; Kwan, W.; Badwal, A.; Puol, T.; Deng, J.Z.; Wang, R.; Ahmed, S.; Mansfield, A.; Fazelzad, R.; Jones, J. Prehabilitation in Adult Cancer Patients Undergoing Chemotherapy or Radiotherapy: A Scoping Review. Cancers 2026, 18, 286. https://doi.org/10.3390/cancers18020286
Type: Review  |  Publication date: 16 January 2026

</li>
<li>Summary: Individuals undergoing cancer treatment often experience side effects like fatigue, muscle loss, and mood changes that can reduce their ability to carry out daily activities. In surgical settings, giving patients a prehabilitation program involving exercise, nutrition, and psychological support prior to treatment helps preserve their strength and quality of life, yet its use for non-surgical treatments remains largely unexamined. Our review therefore examines research on prehabilitation before non-surgical treatments, such as chemotherapy and radiotherapy, to see what kinds of programs exist, how feasible they are, and which patient groups benefit. By mapping the evidence and identifying gaps, we aim to guide clinicians and researchers toward designing better pre-treatment support programs and highlight the need for longer-term trials in diverse and older populations.

</li>
<li>Keywords: prehabilitation; cancer; chemotherapy; radiotherapy; non-surgical treatment</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E15   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/286'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Kwan, D.; Kwan, W.; Badwal, A.; Puol, T.; Deng, J.Z.; Wang, R.; Ahmed, S.; Mansfield, A.; Fazelzad, R.; Jones, J. Prehabilitation in Adult Cancer Patients Undergoing Chemotherapy or Radiotherapy: A Scoping Review. Cancers 2026, 18, 286. https://doi.org/10.3390/cancers18020286<br>
Type: Review  |  Publication date: 16 January 2026<br>
<br>
</li>
<li>Summary: Individuals undergoing cancer treatment often experience side effects like fatigue, muscle loss, and mood changes that can reduce their ability to carry out daily activities. In surgical settings, giving patients a prehabilitation program involving exercise, nutrition, and psychological support prior to treatment helps preserve their strength and quality of life, yet its use for non-surgical treatments remains largely unexamined. Our review therefore examines research on prehabilitation before non-surgical treatments, such as chemotherapy and radiotherapy, to see what kinds of programs exist, how feasible they are, and which patient groups benefit. By mapping the evidence and identifying gaps, we aim to guide clinicians and researchers toward designing better pre-treatment support programs and highlight the need for longer-term trials in diverse and older populations.<br>
<br>
</li>
<li>Keywords: prehabilitation; cancer; chemotherapy; radiotherapy; non-surgical treatment</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/tv9sbqbbdpbk2yxv/E15_-_Prehabilitation_in_Cancer_Care.mp3" length="14061652" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E15   |  10 min   |   Latest   |  Publication Link

Podcast based on: Kwan, D.; Kwan, W.; Badwal, A.; Puol, T.; Deng, J.Z.; Wang, R.; Ahmed, S.; Mansfield, A.; Fazelzad, R.; Jones, J. Prehabilitation in Adult Cancer Patients Undergoing Chemotherapy or Radiotherapy: A Scoping Review. Cancers 2026, 18, 286. https://doi.org/10.3390/cancers18020286Type: Review  |  Publication date: 16 January 2026
Summary: Individuals undergoing cancer treatment often experience side effects like fatigue, muscle loss, and mood changes that can reduce their ability to carry out daily activities. In surgical settings, giving patients a prehabilitation program involving exercise, nutrition, and psychological support prior to treatment helps preserve their strength and quality of life, yet its use for non-surgical treatments remains largely unexamined. Our review therefore examines research on prehabilitation before non-surgical treatments, such as chemotherapy and radiotherapy, to see what kinds of programs exist, how feasible they are, and which patient groups benefit. By mapping the evidence and identifying gaps, we aim to guide clinicians and researchers toward designing better pre-treatment support programs and highlight the need for longer-term trials in diverse and older populations.
Keywords: prehabilitation; cancer; chemotherapy; radiotherapy; non-surgical treatment

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>585</itunes:duration>
                <itunes:episode>15</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E14 - Ultrasound in Skin Cancer</title>
        <itunes:title>E14 - Ultrasound in Skin Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e14-ultrasound-in-skin-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e14-ultrasound-in-skin-cancer/#comments</comments>        <pubDate>Sun, 18 Jan 2026 20:42:50 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/3c069757-dbec-36a6-bd96-5ea1c7c4020f</guid>
                                    <description><![CDATA[<p>E14   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/274'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Szalai, K.; Tóth, K.; Hársing, J.; Gyöngy, M.; Holló, P. High-Frequency Ultrasound Assessment of Basal Cell Carcinoma: Correlations Between Histopathological Subtype, Vascularity, and Age/Sex Distribution. Cancers 2026, 18, 274. https://doi.org/10.3390/cancers18020274
Type: Article  |  Publication date: 15 January 2026

</li>
<li>Summary: Basal cell carcinoma is the most common type of skin cancer and usually grows slowly, but some forms can behave more aggressively. High-frequency ultrasound (HFUS) is a non-invasive imaging method that supports the preoperative evaluation of basal cell carcinoma. In this study, ultrasound contour and vascularity patterns showed a strong association with histological subtype, enabling reliable differentiation between solid and infiltrative tumours. Solid lesions were typically well-defined and hypervascular, whereas infiltrative tumours more often showed irregular margins and reduced vascularity. HFUS therefore represents a valuable adjunct to dermatoscopy for treatment planning and postoperative follow-up.

</li>
<li>Keywords: ultrasound; BCC; HFUS; oncology</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E14   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/274'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Szalai, K.; Tóth, K.; Hársing, J.; Gyöngy, M.; Holló, P. High-Frequency Ultrasound Assessment of Basal Cell Carcinoma: Correlations Between Histopathological Subtype, Vascularity, and Age/Sex Distribution. Cancers 2026, 18, 274. https://doi.org/10.3390/cancers18020274<br>
Type: Article  |  Publication date: 15 January 2026<br>
<br>
</li>
<li>Summary: Basal cell carcinoma is the most common type of skin cancer and usually grows slowly, but some forms can behave more aggressively. High-frequency ultrasound (HFUS) is a non-invasive imaging method that supports the preoperative evaluation of basal cell carcinoma. In this study, ultrasound contour and vascularity patterns showed a strong association with histological subtype, enabling reliable differentiation between solid and infiltrative tumours. Solid lesions were typically well-defined and hypervascular, whereas infiltrative tumours more often showed irregular margins and reduced vascularity. HFUS therefore represents a valuable adjunct to dermatoscopy for treatment planning and postoperative follow-up.<br>
<br>
</li>
<li>Keywords: ultrasound; BCC; HFUS; oncology</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/echfr97epbht6fn4/E14_-_Ultrasound_in_Skin_Cancer.mp3" length="13723732" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E14   |  10 min   |   Latest   |  Publication Link

Podcast based on: Szalai, K.; Tóth, K.; Hársing, J.; Gyöngy, M.; Holló, P. High-Frequency Ultrasound Assessment of Basal Cell Carcinoma: Correlations Between Histopathological Subtype, Vascularity, and Age/Sex Distribution. Cancers 2026, 18, 274. https://doi.org/10.3390/cancers18020274Type: Article  |  Publication date: 15 January 2026
Summary: Basal cell carcinoma is the most common type of skin cancer and usually grows slowly, but some forms can behave more aggressively. High-frequency ultrasound (HFUS) is a non-invasive imaging method that supports the preoperative evaluation of basal cell carcinoma. In this study, ultrasound contour and vascularity patterns showed a strong association with histological subtype, enabling reliable differentiation between solid and infiltrative tumours. Solid lesions were typically well-defined and hypervascular, whereas infiltrative tumours more often showed irregular margins and reduced vascularity. HFUS therefore represents a valuable adjunct to dermatoscopy for treatment planning and postoperative follow-up.
Keywords: ultrasound; BCC; HFUS; oncology

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>571</itunes:duration>
                <itunes:episode>14</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E13 - Glioma Margin Assessment</title>
        <itunes:title>E13 - Glioma Margin Assessment</itunes:title>
        <link>https://podcast.sinapsos.com/e/e13-glioma-margin-assessment/</link>
                    <comments>https://podcast.sinapsos.com/e/e13-glioma-margin-assessment/#comments</comments>        <pubDate>Sun, 18 Jan 2026 20:42:05 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/a823a8e0-2803-33a8-ad69-e24520c0bb8f</guid>
                                    <description><![CDATA[<p>E13   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/263'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Tykocki, T.; Rakasz, Ł. Intraoperative Spectroscopic and Mass Spectrometric Assessment of Glioma Margins: A Systematic Review and Meta-Analysis. Cancers 2026, 18, 263. https://doi.org/10.3390/cancers18020263
Type: Systematic Review  |  Publication date: 14 January 2026

</li>
<li>Summary: Maximal safe removal of gliomas is crucial for improving patient survival, yet surgeons often face difficulty distinguishing tumor tissue from normal brain tissue during surgery. Traditional frozen-section analysis is accurate but slow and disrupts operative workflow. This systematic review and meta-analysis evaluated three emerging, label-free intraoperative technologies—Raman spectroscopy, mass spectrometry, and optical coherence tomography—that provide real-time biochemical or structural information to guide tumor resection. By analyzing 24 human studies involving nearly 1800 patients, we found that these techniques achieve high diagnostic accuracy in identifying tumor tissue, infiltrated margins, and key molecular features such as IDH mutation status. Raman spectroscopy and mass spectrometry showed the strongest overall performance, outperforming optical coherence tomography. Importantly, these methods offer rapid, objective feedback without interrupting surgery, supporting more precise glioma resection. Our findings indicate that real-time spectroscopic and molecular diagnostics are ready for broader clinical integration and may enhance surgical decision-making in modern neuro-oncology.

</li>
<li>Keywords: glioma; Raman spectroscopy; mass spectrometry; optical coherence tomography; intraoperative diagnostics; IDH mutation</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E13   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/263'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Tykocki, T.; Rakasz, Ł. Intraoperative Spectroscopic and Mass Spectrometric Assessment of Glioma Margins: A Systematic Review and Meta-Analysis. Cancers 2026, 18, 263. https://doi.org/10.3390/cancers18020263<br>
Type: Systematic Review  |  Publication date: 14 January 2026<br>
<br>
</li>
<li>Summary: Maximal safe removal of gliomas is crucial for improving patient survival, yet surgeons often face difficulty distinguishing tumor tissue from normal brain tissue during surgery. Traditional frozen-section analysis is accurate but slow and disrupts operative workflow. This systematic review and meta-analysis evaluated three emerging, label-free intraoperative technologies—Raman spectroscopy, mass spectrometry, and optical coherence tomography—that provide real-time biochemical or structural information to guide tumor resection. By analyzing 24 human studies involving nearly 1800 patients, we found that these techniques achieve high diagnostic accuracy in identifying tumor tissue, infiltrated margins, and key molecular features such as IDH mutation status. Raman spectroscopy and mass spectrometry showed the strongest overall performance, outperforming optical coherence tomography. Importantly, these methods offer rapid, objective feedback without interrupting surgery, supporting more precise glioma resection. Our findings indicate that real-time spectroscopic and molecular diagnostics are ready for broader clinical integration and may enhance surgical decision-making in modern neuro-oncology.<br>
<br>
</li>
<li>Keywords: glioma; Raman spectroscopy; mass spectrometry; optical coherence tomography; intraoperative diagnostics; IDH mutation</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/pdeha75byz3tm8mn/E13_-_Glioma_Margin_Assessment.mp3" length="14466028" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E13   |  11 min   |   Latest   |  Publication Link

Podcast based on: Tykocki, T.; Rakasz, Ł. Intraoperative Spectroscopic and Mass Spectrometric Assessment of Glioma Margins: A Systematic Review and Meta-Analysis. Cancers 2026, 18, 263. https://doi.org/10.3390/cancers18020263Type: Systematic Review  |  Publication date: 14 January 2026
Summary: Maximal safe removal of gliomas is crucial for improving patient survival, yet surgeons often face difficulty distinguishing tumor tissue from normal brain tissue during surgery. Traditional frozen-section analysis is accurate but slow and disrupts operative workflow. This systematic review and meta-analysis evaluated three emerging, label-free intraoperative technologies—Raman spectroscopy, mass spectrometry, and optical coherence tomography—that provide real-time biochemical or structural information to guide tumor resection. By analyzing 24 human studies involving nearly 1800 patients, we found that these techniques achieve high diagnostic accuracy in identifying tumor tissue, infiltrated margins, and key molecular features such as IDH mutation status. Raman spectroscopy and mass spectrometry showed the strongest overall performance, outperforming optical coherence tomography. Importantly, these methods offer rapid, objective feedback without interrupting surgery, supporting more precise glioma resection. Our findings indicate that real-time spectroscopic and molecular diagnostics are ready for broader clinical integration and may enhance surgical decision-making in modern neuro-oncology.
Keywords: glioma; Raman spectroscopy; mass spectrometry; optical coherence tomography; intraoperative diagnostics; IDH mutation

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>602</itunes:duration>
                <itunes:episode>13</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E12 - Endometrial Cancer Classification</title>
        <itunes:title>E12 - Endometrial Cancer Classification</itunes:title>
        <link>https://podcast.sinapsos.com/e/e12-endometrial-cancer-classification/</link>
                    <comments>https://podcast.sinapsos.com/e/e12-endometrial-cancer-classification/#comments</comments>        <pubDate>Sun, 18 Jan 2026 20:41:21 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/fd7ca76a-22ac-3824-b1ee-1b7d7686e7aa</guid>
                                    <description><![CDATA[<p>E12   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/247'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Restaino, S.; Pellecchia, G.; Arcieri, M.; Mariuzzi, L.; Orsaria, M.; Tulisso, A.; Cesselli, D.; Bulfoni, M.; Poli, A.; Paparcura, F.; Bogani, G.; Mariani, A.; Zannoni, G.; Scambia, G.; Vizzielli, G. Alignment of Molecular Classification Between Diagnosis and Recurrence in Endometrial Cancer: Lessons from a Single-Institution Experience to Inform Future Pathways. Cancers 2026, 18, 247. https://doi.org/10.3390/cancers18020247
Type: Article  |  Publication date: 13 January 2026

</li>
<li>Summary: Endometrial cancer treatment and prognosis have greatly improved thanks to advances in understanding its molecular profile. However, it is still unclear whether these molecular characteristics remain stable over time, particularly when the disease returns after initial treatment. This study explores the concordance and potential evolution of molecular classification between primary diagnosis and recurrence in endometrial cancer, building upon emerging evidence that has begun to address this question. This study explores the concordance and potential evolution of molecular classification between primary diagnosis and recurrence in endometrial cancer, building upon emerging evidence that has begun to address this question. By examining this relationship, our research provides valuable preliminary data that could guide future studies on the biological behavior of recurrent disease. These insights may ultimately contribute to more precise and personalized treatment strategies for patients with endometrial cancer.

</li>
<li>Keywords: molecular biology; endometrial cancer; recurrence</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E12   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/247'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Restaino, S.; Pellecchia, G.; Arcieri, M.; Mariuzzi, L.; Orsaria, M.; Tulisso, A.; Cesselli, D.; Bulfoni, M.; Poli, A.; Paparcura, F.; Bogani, G.; Mariani, A.; Zannoni, G.; Scambia, G.; Vizzielli, G. Alignment of Molecular Classification Between Diagnosis and Recurrence in Endometrial Cancer: Lessons from a Single-Institution Experience to Inform Future Pathways. Cancers 2026, 18, 247. https://doi.org/10.3390/cancers18020247<br>
Type: Article  |  Publication date: 13 January 2026<br>
<br>
</li>
<li>Summary: Endometrial cancer treatment and prognosis have greatly improved thanks to advances in understanding its molecular profile. However, it is still unclear whether these molecular characteristics remain stable over time, particularly when the disease returns after initial treatment. This study explores the concordance and potential evolution of molecular classification between primary diagnosis and recurrence in endometrial cancer, building upon emerging evidence that has begun to address this question. This study explores the concordance and potential evolution of molecular classification between primary diagnosis and recurrence in endometrial cancer, building upon emerging evidence that has begun to address this question. By examining this relationship, our research provides valuable preliminary data that could guide future studies on the biological behavior of recurrent disease. These insights may ultimately contribute to more precise and personalized treatment strategies for patients with endometrial cancer.<br>
<br>
</li>
<li>Keywords: molecular biology; endometrial cancer; recurrence</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/r4spcptnxtr8k5e4/E12_-_Endometrial_Cancer_Classification.mp3" length="13527501" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E12   |  10 min   |   Latest   |  Publication Link

Podcast based on: Restaino, S.; Pellecchia, G.; Arcieri, M.; Mariuzzi, L.; Orsaria, M.; Tulisso, A.; Cesselli, D.; Bulfoni, M.; Poli, A.; Paparcura, F.; Bogani, G.; Mariani, A.; Zannoni, G.; Scambia, G.; Vizzielli, G. Alignment of Molecular Classification Between Diagnosis and Recurrence in Endometrial Cancer: Lessons from a Single-Institution Experience to Inform Future Pathways. Cancers 2026, 18, 247. https://doi.org/10.3390/cancers18020247Type: Article  |  Publication date: 13 January 2026
Summary: Endometrial cancer treatment and prognosis have greatly improved thanks to advances in understanding its molecular profile. However, it is still unclear whether these molecular characteristics remain stable over time, particularly when the disease returns after initial treatment. This study explores the concordance and potential evolution of molecular classification between primary diagnosis and recurrence in endometrial cancer, building upon emerging evidence that has begun to address this question. This study explores the concordance and potential evolution of molecular classification between primary diagnosis and recurrence in endometrial cancer, building upon emerging evidence that has begun to address this question. By examining this relationship, our research provides valuable preliminary data that could guide future studies on the biological behavior of recurrent disease. These insights may ultimately contribute to more precise and personalized treatment strategies for patients with endometrial cancer.
Keywords: molecular biology; endometrial cancer; recurrence

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>563</itunes:duration>
                <itunes:episode>12</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E11 - Fibroblasts in Pancreatic Cancer</title>
        <itunes:title>E11 - Fibroblasts in Pancreatic Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e11-fibroblasts-in-pancreatic-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e11-fibroblasts-in-pancreatic-cancer/#comments</comments>        <pubDate>Sun, 18 Jan 2026 20:40:37 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/176d5b0e-b53d-377a-ad28-2e8851d3809a</guid>
                                    <description><![CDATA[<p>E11   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/233'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Rupert, J.; Cai, L.; Daquinag, A.C.; Anastassiou, D.; Kolonin, M.G. Adipose Stromal Cell-Derived Cancer-Associated Fibroblasts Promote Pancreatic Adenocarcinoma Progression Through SFRP4 Signaling. Cancers 2026, 18, 233. https://doi.org/10.3390/cancers18020233
Type: Article  |  Publication date: 12 January 2026

</li>
<li>Summary: Cancer-associated fibroblasts (CAFs) promote the progression of pancreatic ductal adenocarcinoma by remodeling the microenvironment toward tumor growth, invasion, and metastasis. A sub-population of CAFs originates from adipose stromal cells in adjacent fat tissue through mechanisms that are not well understood. Using co-cultures of human adipose stromal cells with pancreatic cancer cells and a mouse model of pancreatic cancer, we found that tumor cells induce Wnt and TGFβ signaling and extracellular matrix gene expression in adipose stromal cells. We discovered that two important genes, the long non-coding RNA LINC01614 and the Wnt signaling modulator SFRP4, are required for this transition. Loss of SFRP4 reduced cancer cell migration, growth, and metastasis, suggesting that SFRP4 is a promising therapeutic target inhibiting the transition.

</li>
<li>Keywords: cancer; tumor microenvironment; metastasis; pancreas; fibroblast; stromal; adipose; LINC01614; SFRP4; Wnt; TGF; SMAD</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E11   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/233'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Rupert, J.; Cai, L.; Daquinag, A.C.; Anastassiou, D.; Kolonin, M.G. Adipose Stromal Cell-Derived Cancer-Associated Fibroblasts Promote Pancreatic Adenocarcinoma Progression Through SFRP4 Signaling. Cancers 2026, 18, 233. https://doi.org/10.3390/cancers18020233<br>
Type: Article  |  Publication date: 12 January 2026<br>
<br>
</li>
<li>Summary: Cancer-associated fibroblasts (CAFs) promote the progression of pancreatic ductal adenocarcinoma by remodeling the microenvironment toward tumor growth, invasion, and metastasis. A sub-population of CAFs originates from adipose stromal cells in adjacent fat tissue through mechanisms that are not well understood. Using co-cultures of human adipose stromal cells with pancreatic cancer cells and a mouse model of pancreatic cancer, we found that tumor cells induce Wnt and TGFβ signaling and extracellular matrix gene expression in adipose stromal cells. We discovered that two important genes, the long non-coding RNA LINC01614 and the Wnt signaling modulator SFRP4, are required for this transition. Loss of SFRP4 reduced cancer cell migration, growth, and metastasis, suggesting that SFRP4 is a promising therapeutic target inhibiting the transition.<br>
<br>
</li>
<li>Keywords: cancer; tumor microenvironment; metastasis; pancreas; fibroblast; stromal; adipose; LINC01614; SFRP4; Wnt; TGF; SMAD</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/rbxgrbkykt4x7bkp/E11_-_Fibroblasts_in_Pancreatic_Cancer.mp3" length="16162524" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E11   |  12 min   |   Latest   |  Publication Link

Podcast based on: Rupert, J.; Cai, L.; Daquinag, A.C.; Anastassiou, D.; Kolonin, M.G. Adipose Stromal Cell-Derived Cancer-Associated Fibroblasts Promote Pancreatic Adenocarcinoma Progression Through SFRP4 Signaling. Cancers 2026, 18, 233. https://doi.org/10.3390/cancers18020233Type: Article  |  Publication date: 12 January 2026
Summary: Cancer-associated fibroblasts (CAFs) promote the progression of pancreatic ductal adenocarcinoma by remodeling the microenvironment toward tumor growth, invasion, and metastasis. A sub-population of CAFs originates from adipose stromal cells in adjacent fat tissue through mechanisms that are not well understood. Using co-cultures of human adipose stromal cells with pancreatic cancer cells and a mouse model of pancreatic cancer, we found that tumor cells induce Wnt and TGFβ signaling and extracellular matrix gene expression in adipose stromal cells. We discovered that two important genes, the long non-coding RNA LINC01614 and the Wnt signaling modulator SFRP4, are required for this transition. Loss of SFRP4 reduced cancer cell migration, growth, and metastasis, suggesting that SFRP4 is a promising therapeutic target inhibiting the transition.
Keywords: cancer; tumor microenvironment; metastasis; pancreas; fibroblast; stromal; adipose; LINC01614; SFRP4; Wnt; TGF; SMAD

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>673</itunes:duration>
                <itunes:episode>11</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E10 - Breathprints for Breast Cancer Risk</title>
        <itunes:title>E10 - Breathprints for Breast Cancer Risk</itunes:title>
        <link>https://podcast.sinapsos.com/e/e10-breathprints-for-breast-cancer-risk/</link>
                    <comments>https://podcast.sinapsos.com/e/e10-breathprints-for-breast-cancer-risk/#comments</comments>        <pubDate>Sun, 18 Jan 2026 20:39:52 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/4925cd48-e181-3307-af73-d39827b50ed5</guid>
                                    <description><![CDATA[<p>E10   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/226'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Masilamani, A.P.; Hooper, J.K.; Rahman, M.H.; Philip, R.; Kaushik, P.; Graham, G.; Yockell-Lelievre, H.; Khomami Abadi, M.; Meterissian, S.H. Breathprints for Breast Cancer: Evaluating a Non-Invasive Approach to BI-RADS 4 Risk Stratification in a Preliminary Study. Cancers 2026, 18, 226. https://doi.org/10.3390/cancers18020226
Type: Article  |  Publication date: 11 January 2026

</li>
<li>Summary: Breast cancer screening often identifies findings that are suspicious but uncertain, especially those labeled as BI-RADS 4. While doctors usually recommend a biopsy for these cases, most turn out to be benign, meaning many women go through an invasive procedure unnecessarily. This study explored whether a simple breath test could help better identify high-risk patients. By analyzing patterns of natural chemicals in exhaled breath, we trained a computer model to distinguish between cancerous and non-cancerous findings. The model was able to correctly identify most cancers while also giving strong reassurance when no cancer was present. These results suggest that a breath test could be used alongside mammography to provide patients and doctors with clearer information. If confirmed in larger studies, this approach could spare many women from unnecessary biopsies, lower healthcare costs, and improve trust in breast cancer screening.

</li>
<li>Keywords: breast cancer; BI-RADS 4; breath analysis; volatile organic compounds (VOCs); digital olfaction (electronic nose); chemiresistive sensor array; machine learning; multi-modal fusion; autoencoder; risk stratification; rule-out diagnostics</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E10   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/226'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Masilamani, A.P.; Hooper, J.K.; Rahman, M.H.; Philip, R.; Kaushik, P.; Graham, G.; Yockell-Lelievre, H.; Khomami Abadi, M.; Meterissian, S.H. Breathprints for Breast Cancer: Evaluating a Non-Invasive Approach to BI-RADS 4 Risk Stratification in a Preliminary Study. Cancers 2026, 18, 226. https://doi.org/10.3390/cancers18020226<br>
Type: Article  |  Publication date: 11 January 2026<br>
<br>
</li>
<li>Summary: Breast cancer screening often identifies findings that are suspicious but uncertain, especially those labeled as BI-RADS 4. While doctors usually recommend a biopsy for these cases, most turn out to be benign, meaning many women go through an invasive procedure unnecessarily. This study explored whether a simple breath test could help better identify high-risk patients. By analyzing patterns of natural chemicals in exhaled breath, we trained a computer model to distinguish between cancerous and non-cancerous findings. The model was able to correctly identify most cancers while also giving strong reassurance when no cancer was present. These results suggest that a breath test could be used alongside mammography to provide patients and doctors with clearer information. If confirmed in larger studies, this approach could spare many women from unnecessary biopsies, lower healthcare costs, and improve trust in breast cancer screening.<br>
<br>
</li>
<li>Keywords: breast cancer; BI-RADS 4; breath analysis; volatile organic compounds (VOCs); digital olfaction (electronic nose); chemiresistive sensor array; machine learning; multi-modal fusion; autoencoder; risk stratification; rule-out diagnostics</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/85jjv2zyut6dbz6e/E10_-_Breathprints_for_Breast_Cancer_Risk.mp3" length="15334965" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E10   |  11 min   |   Latest   |  Publication Link

Podcast based on: Masilamani, A.P.; Hooper, J.K.; Rahman, M.H.; Philip, R.; Kaushik, P.; Graham, G.; Yockell-Lelievre, H.; Khomami Abadi, M.; Meterissian, S.H. Breathprints for Breast Cancer: Evaluating a Non-Invasive Approach to BI-RADS 4 Risk Stratification in a Preliminary Study. Cancers 2026, 18, 226. https://doi.org/10.3390/cancers18020226Type: Article  |  Publication date: 11 January 2026
Summary: Breast cancer screening often identifies findings that are suspicious but uncertain, especially those labeled as BI-RADS 4. While doctors usually recommend a biopsy for these cases, most turn out to be benign, meaning many women go through an invasive procedure unnecessarily. This study explored whether a simple breath test could help better identify high-risk patients. By analyzing patterns of natural chemicals in exhaled breath, we trained a computer model to distinguish between cancerous and non-cancerous findings. The model was able to correctly identify most cancers while also giving strong reassurance when no cancer was present. These results suggest that a breath test could be used alongside mammography to provide patients and doctors with clearer information. If confirmed in larger studies, this approach could spare many women from unnecessary biopsies, lower healthcare costs, and improve trust in breast cancer screening.
Keywords: breast cancer; BI-RADS 4; breath analysis; volatile organic compounds (VOCs); digital olfaction (electronic nose); chemiresistive sensor array; machine learning; multi-modal fusion; autoencoder; risk stratification; rule-out diagnostics

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>638</itunes:duration>
                <itunes:episode>10</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E9 - Radiation-Induced Mesothelioma</title>
        <itunes:title>E9 - Radiation-Induced Mesothelioma</itunes:title>
        <link>https://podcast.sinapsos.com/e/e9-radiationinduced-mesothelioma/</link>
                    <comments>https://podcast.sinapsos.com/e/e9-radiationinduced-mesothelioma/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:33:19 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/73c8fd69-546a-3844-8b38-01cc76916690</guid>
                                    <description><![CDATA[<p>E9   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/221'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Fujita, N.; Fujita, K.; Osumi, H.; Takefuji, Y. The Diagnostic Trap in Radiation-Induced Mesothelioma: Kinetic-Morphological Decoupling Masks Molecular Aggression. Cancers 2026, 18, 221. https://doi.org/10.3390/cancers18020221
Type: Article  |  Publication date: 09 January 2026

</li>
<li>Summary: Typically, the microscopic appearance of a tumor predicts its biological aggression. However, in malignant pleural mesothelioma caused by radiation, our analysis of 20 rare cases without asbestos exposure suggests that this rule can be clinically deceptive. In this cohort, the intensity of radiotherapy doses appears to shape how the cancer evolves: moderate doses were associated with gradual, age-dependent latent periods, while high doses were associated with rapid, aggressive onset. Paradoxically, these aggressive high-dose tumors retained an indolent-appearing morphology, presenting a potential diagnostic trap that masks their true nature. We propose that reviewing a patient’s radiotherapy history could help expose this discrepancy, potentially guiding risk-stratified precision therapy.

</li>
<li>Keywords: malignant pleural mesothelioma; radiation-induced cancer; kinetic-morphological decoupling; diagnostic trap; CDK4/6 inhibitors; ; chromothripsis; tumor suppressor genes; precision medicine; therapeutic stratification; CSU Beagle Study</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E9   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/221'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Fujita, N.; Fujita, K.; Osumi, H.; Takefuji, Y. The Diagnostic Trap in Radiation-Induced Mesothelioma: Kinetic-Morphological Decoupling Masks Molecular Aggression. Cancers 2026, 18, 221. https://doi.org/10.3390/cancers18020221<br>
Type: Article  |  Publication date: 09 January 2026<br>
<br>
</li>
<li>Summary: Typically, the microscopic appearance of a tumor predicts its biological aggression. However, in malignant pleural mesothelioma caused by radiation, our analysis of 20 rare cases without asbestos exposure suggests that this rule can be clinically deceptive. In this cohort, the intensity of radiotherapy doses appears to shape how the cancer evolves: moderate doses were associated with gradual, age-dependent latent periods, while high doses were associated with rapid, aggressive onset. Paradoxically, these aggressive high-dose tumors retained an indolent-appearing morphology, presenting a potential diagnostic trap that masks their true nature. We propose that reviewing a patient’s radiotherapy history could help expose this discrepancy, potentially guiding risk-stratified precision therapy.<br>
<br>
</li>
<li>Keywords: malignant pleural mesothelioma; radiation-induced cancer; kinetic-morphological decoupling; diagnostic trap; CDK4/6 inhibitors; ; chromothripsis; tumor suppressor genes; precision medicine; therapeutic stratification; CSU Beagle Study</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/r8vyznghghre9ats/E9_-_RadiationInduced_Mesothelioma.mp3" length="14220268" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E9   |  10 min   |   Latest   |  Publication Link

Podcast based on: Fujita, N.; Fujita, K.; Osumi, H.; Takefuji, Y. The Diagnostic Trap in Radiation-Induced Mesothelioma: Kinetic-Morphological Decoupling Masks Molecular Aggression. Cancers 2026, 18, 221. https://doi.org/10.3390/cancers18020221Type: Article  |  Publication date: 09 January 2026
Summary: Typically, the microscopic appearance of a tumor predicts its biological aggression. However, in malignant pleural mesothelioma caused by radiation, our analysis of 20 rare cases without asbestos exposure suggests that this rule can be clinically deceptive. In this cohort, the intensity of radiotherapy doses appears to shape how the cancer evolves: moderate doses were associated with gradual, age-dependent latent periods, while high doses were associated with rapid, aggressive onset. Paradoxically, these aggressive high-dose tumors retained an indolent-appearing morphology, presenting a potential diagnostic trap that masks their true nature. We propose that reviewing a patient’s radiotherapy history could help expose this discrepancy, potentially guiding risk-stratified precision therapy.
Keywords: malignant pleural mesothelioma; radiation-induced cancer; kinetic-morphological decoupling; diagnostic trap; CDK4/6 inhibitors; ; chromothripsis; tumor suppressor genes; precision medicine; therapeutic stratification; CSU Beagle Study

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>592</itunes:duration>
                <itunes:episode>9</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E8 - Autophagy in Cancer Cell Death</title>
        <itunes:title>E8 - Autophagy in Cancer Cell Death</itunes:title>
        <link>https://podcast.sinapsos.com/e/e8-autophagy-in-cancer-cell-death/</link>
                    <comments>https://podcast.sinapsos.com/e/e8-autophagy-in-cancer-cell-death/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:32:40 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/b0a52780-b524-3087-bf73-6576a82b4b0e</guid>
                                    <description><![CDATA[<p>E8   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/205'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Matsushita, M.; Moriwaki, M. Autophagy Modulates Immunogenic Cell Death in Cancer. Cancers 2026, 18, 205. https://doi.org/10.3390/cancers18020205
Type: Review  |  Publication date: 08 January 2026

</li>
<li>Summary: Immunogenic cell death (ICD) is a form of regulated cell death that could change a “cold” tumor into an immune-inflamed “hot” tumor by exposing and releasing damage-associated molecular patterns (DAMPs). Recent works indicate that autophagy can either facilitate or inhibit ICD, depending on the context and which step of the pathway is targeted. In this review, we summarize the current knowledge on the autophagy–ICD axis in various kinds of cancer, and we then focus on hematological malignancies, especially multiple myeloma, in which autophagy and ICD play important roles. We propose how the phase-specific modulation of autophagy could be exploited to design novel immunogenic chemotherapy combinations and improve cellular immunotherapies.

</li>
<li>Keywords: autophagy; immunogenic cell death; damage-associated molecular patterns; tumor microenvironment; multiple myeloma</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E8   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/205'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Matsushita, M.; Moriwaki, M. Autophagy Modulates Immunogenic Cell Death in Cancer. Cancers 2026, 18, 205. https://doi.org/10.3390/cancers18020205<br>
Type: Review  |  Publication date: 08 January 2026<br>
<br>
</li>
<li>Summary: Immunogenic cell death (ICD) is a form of regulated cell death that could change a “cold” tumor into an immune-inflamed “hot” tumor by exposing and releasing damage-associated molecular patterns (DAMPs). Recent works indicate that autophagy can either facilitate or inhibit ICD, depending on the context and which step of the pathway is targeted. In this review, we summarize the current knowledge on the autophagy–ICD axis in various kinds of cancer, and we then focus on hematological malignancies, especially multiple myeloma, in which autophagy and ICD play important roles. We propose how the phase-specific modulation of autophagy could be exploited to design novel immunogenic chemotherapy combinations and improve cellular immunotherapies.<br>
<br>
</li>
<li>Keywords: autophagy; immunogenic cell death; damage-associated molecular patterns; tumor microenvironment; multiple myeloma</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/bxz7995bnffczg8s/E8_-_Autophagy_in_Cancer_Cell_Death.mp3" length="19474642" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E8   |  14 min   |   Latest   |  Publication Link

Podcast based on: Matsushita, M.; Moriwaki, M. Autophagy Modulates Immunogenic Cell Death in Cancer. Cancers 2026, 18, 205. https://doi.org/10.3390/cancers18020205Type: Review  |  Publication date: 08 January 2026
Summary: Immunogenic cell death (ICD) is a form of regulated cell death that could change a “cold” tumor into an immune-inflamed “hot” tumor by exposing and releasing damage-associated molecular patterns (DAMPs). Recent works indicate that autophagy can either facilitate or inhibit ICD, depending on the context and which step of the pathway is targeted. In this review, we summarize the current knowledge on the autophagy–ICD axis in various kinds of cancer, and we then focus on hematological malignancies, especially multiple myeloma, in which autophagy and ICD play important roles. We propose how the phase-specific modulation of autophagy could be exploited to design novel immunogenic chemotherapy combinations and improve cellular immunotherapies.
Keywords: autophagy; immunogenic cell death; damage-associated molecular patterns; tumor microenvironment; multiple myeloma

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>811</itunes:duration>
                <itunes:episode>8</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E7 - Minimally Invasive Pancreatic Surgery</title>
        <itunes:title>E7 - Minimally Invasive Pancreatic Surgery</itunes:title>
        <link>https://podcast.sinapsos.com/e/e7-minimally-invasive-pancreatic-surgery/</link>
                    <comments>https://podcast.sinapsos.com/e/e7-minimally-invasive-pancreatic-surgery/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:32:07 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/d6036135-9ca5-3e10-893a-59a30bf7a9f2</guid>
                                    <description><![CDATA[<p>E7   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/197'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Choi, M.; Kang, C.M. Minimally Invasive Pancreatoduodenectomy for Pancreatic Cancer: Current Perspectives and Future Directions. Cancers 2026, 18, 197. https://doi.org/10.3390/cancers18020197
Type: Review  |  Publication date: 07 January 2026

</li>
<li>Summary: Minimally invasive pancreatoduodenectomy has emerged as a feasible option for pancreatic cancer in expert centers. Current evidence shows comparable safety and oncologic adequacy to open surgery in selected patients, while long-term PDAC-specific data and standardization remain needed.

</li>
<li>Keywords: minimally invasive surgery; pancreatoduodenectomy; pancreatic cancer; laparoscopy; robotic surgery</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E7   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/197'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Choi, M.; Kang, C.M. Minimally Invasive Pancreatoduodenectomy for Pancreatic Cancer: Current Perspectives and Future Directions. Cancers 2026, 18, 197. https://doi.org/10.3390/cancers18020197<br>
Type: Review  |  Publication date: 07 January 2026<br>
<br>
</li>
<li>Summary: Minimally invasive pancreatoduodenectomy has emerged as a feasible option for pancreatic cancer in expert centers. Current evidence shows comparable safety and oncologic adequacy to open surgery in selected patients, while long-term PDAC-specific data and standardization remain needed.<br>
<br>
</li>
<li>Keywords: minimally invasive surgery; pancreatoduodenectomy; pancreatic cancer; laparoscopy; robotic surgery</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/88cye6jccfcb8gd6/E7_-_Minimally_Invasive_Pancreatic_Surgery_E7_-_Minimally_Inva9te9b.mp3" length="16076634" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E7   |  12 min   |   Latest   |  Publication Link

Podcast based on: Choi, M.; Kang, C.M. Minimally Invasive Pancreatoduodenectomy for Pancreatic Cancer: Current Perspectives and Future Directions. Cancers 2026, 18, 197. https://doi.org/10.3390/cancers18020197Type: Review  |  Publication date: 07 January 2026
Summary: Minimally invasive pancreatoduodenectomy has emerged as a feasible option for pancreatic cancer in expert centers. Current evidence shows comparable safety and oncologic adequacy to open surgery in selected patients, while long-term PDAC-specific data and standardization remain needed.
Keywords: minimally invasive surgery; pancreatoduodenectomy; pancreatic cancer; laparoscopy; robotic surgery

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>669</itunes:duration>
                <itunes:episode>7</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E6 - Romiplostim in Lymphoma</title>
        <itunes:title>E6 - Romiplostim in Lymphoma</itunes:title>
        <link>https://podcast.sinapsos.com/e/e6-romiplostim-in-lymphoma/</link>
                    <comments>https://podcast.sinapsos.com/e/e6-romiplostim-in-lymphoma/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:31:34 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/48b9c356-ad56-3f0f-998c-41dd1b3acd62</guid>
                                    <description><![CDATA[<p>E6   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/188'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Joffe, E.; Epstein-Peterson, Z.; Falchi, L.; Noy, A.; Zelenetz, A.D.; Owens, C.; Gilbert, L.; Salles, G.; Soff, G.A. Romiplostim for Prevention of Severe Chemotherapy-Induced Thrombocytopenia in Lymphoma Patients—Phase I Study. Cancers 2026, 18, 188. https://doi.org/10.3390/cancers18020188
Type: Article  |  Publication date: 06 January 2026

</li>
<li>Summary: Lymphoma patients receiving intensive chemotherapy frequently develop severe chemotherapy-induced thrombocytopenia, characterized by critically low platelets that increase bleeding risk, necessitate platelet transfusions, and often force treatment delays or dose reductions. While pharmacologic growth factors are routinely used to manage chemotherapy-induced neutropenia, thrombopoietic agents remain inadequately studied. This phase I study investigated whether secondary prophylaxis with weekly romiplostim administration could prevent recurrent severe thrombocytopenia in lymphoma patients undergoing chemotherapy who had already experienced profound platelet drops requiring transfusions in prior cycles. Nine patients were enrolled across three dose schedules to establish a recommended phase 2 dose schedule. Romiplostim effectively prevented grade 4 thrombocytopenia in nearly half of the chemotherapy cycles and substantially reduced platelet transfusion requirements in this high-risk population. The agent was well-tolerated without thromboembolic complications, enabling most patients to maintain their planned chemotherapy schedule at full dose intensity. These findings establish a dosing framework and suggest that secondary prophylaxis with romiplostim may represent a viable strategy to optimize chemotherapy delivery in lymphoma patients.

</li>
<li>Keywords: severe chemotherapy induced thrombocytopenia; lymphoma; romiplostim</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E6   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/2/188'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Joffe, E.; Epstein-Peterson, Z.; Falchi, L.; Noy, A.; Zelenetz, A.D.; Owens, C.; Gilbert, L.; Salles, G.; Soff, G.A. Romiplostim for Prevention of Severe Chemotherapy-Induced Thrombocytopenia in Lymphoma Patients—Phase I Study. Cancers 2026, 18, 188. https://doi.org/10.3390/cancers18020188<br>
Type: Article  |  Publication date: 06 January 2026<br>
<br>
</li>
<li>Summary: Lymphoma patients receiving intensive chemotherapy frequently develop severe chemotherapy-induced thrombocytopenia, characterized by critically low platelets that increase bleeding risk, necessitate platelet transfusions, and often force treatment delays or dose reductions. While pharmacologic growth factors are routinely used to manage chemotherapy-induced neutropenia, thrombopoietic agents remain inadequately studied. This phase I study investigated whether secondary prophylaxis with weekly romiplostim administration could prevent recurrent severe thrombocytopenia in lymphoma patients undergoing chemotherapy who had already experienced profound platelet drops requiring transfusions in prior cycles. Nine patients were enrolled across three dose schedules to establish a recommended phase 2 dose schedule. Romiplostim effectively prevented grade 4 thrombocytopenia in nearly half of the chemotherapy cycles and substantially reduced platelet transfusion requirements in this high-risk population. The agent was well-tolerated without thromboembolic complications, enabling most patients to maintain their planned chemotherapy schedule at full dose intensity. These findings establish a dosing framework and suggest that secondary prophylaxis with romiplostim may represent a viable strategy to optimize chemotherapy delivery in lymphoma patients.<br>
<br>
</li>
<li>Keywords: severe chemotherapy induced thrombocytopenia; lymphoma; romiplostim</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/bxqdvf5ruphafpe3/E6_-_Romiplostim_in_Lymphoma.mp3" length="15868490" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E6   |  12 min   |   Latest   |  Publication Link

Podcast based on: Joffe, E.; Epstein-Peterson, Z.; Falchi, L.; Noy, A.; Zelenetz, A.D.; Owens, C.; Gilbert, L.; Salles, G.; Soff, G.A. Romiplostim for Prevention of Severe Chemotherapy-Induced Thrombocytopenia in Lymphoma Patients—Phase I Study. Cancers 2026, 18, 188. https://doi.org/10.3390/cancers18020188Type: Article  |  Publication date: 06 January 2026
Summary: Lymphoma patients receiving intensive chemotherapy frequently develop severe chemotherapy-induced thrombocytopenia, characterized by critically low platelets that increase bleeding risk, necessitate platelet transfusions, and often force treatment delays or dose reductions. While pharmacologic growth factors are routinely used to manage chemotherapy-induced neutropenia, thrombopoietic agents remain inadequately studied. This phase I study investigated whether secondary prophylaxis with weekly romiplostim administration could prevent recurrent severe thrombocytopenia in lymphoma patients undergoing chemotherapy who had already experienced profound platelet drops requiring transfusions in prior cycles. Nine patients were enrolled across three dose schedules to establish a recommended phase 2 dose schedule. Romiplostim effectively prevented grade 4 thrombocytopenia in nearly half of the chemotherapy cycles and substantially reduced platelet transfusion requirements in this high-risk population. The agent was well-tolerated without thromboembolic complications, enabling most patients to maintain their planned chemotherapy schedule at full dose intensity. These findings establish a dosing framework and suggest that secondary prophylaxis with romiplostim may represent a viable strategy to optimize chemotherapy delivery in lymphoma patients.
Keywords: severe chemotherapy induced thrombocytopenia; lymphoma; romiplostim

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
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        <itunes:block>No</itunes:block>
        <itunes:duration>661</itunes:duration>
                <itunes:episode>6</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E5 - Glioblastoma Survival in Elderly</title>
        <itunes:title>E5 - Glioblastoma Survival in Elderly</itunes:title>
        <link>https://podcast.sinapsos.com/e/e5-glioblastoma-survival-in-elderly/</link>
                    <comments>https://podcast.sinapsos.com/e/e5-glioblastoma-survival-in-elderly/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:30:56 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/5e70fdf6-820e-3779-a39c-acb9b90618a6</guid>
                                    <description><![CDATA[<p>E5   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/178'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Ali, A.M.S.; Parmar, V.; Hannan, C.J.; Farah, J.O. Predictors of Survival in Patients Aged ≥70 with Glioblastoma: A Time-Dependent Multivariable Analysis. Cancers 2026, 18, 178. https://doi.org/10.3390/cancers18010178
Type: Article  |  Publication date: 05 January 2026

</li>
<li>Summary: Glioblastoma is an aggressive brain tumour with a very poor outlook, particularly in older patients, and its incidence is expected to rise as the population ages. This study reviewed the outcomes of 124 patients aged 70 years or older who underwent surgery for glioblastoma at a single specialist neurosurgical centre between 2021 and 2025, with the aim of identifying factors linked to survival. Overall survival remained limited, with a median survival of around 8 months. Two factors were clearly associated with longer survival. Patients who received chemotherapy and radiotherapy after surgery lived longer than those who did not, with the benefit being strongest in the early months following surgery and gradually reducing over time. In addition, patients in whom all visible tumour could be removed during surgery tended to live longer than those who had only partial tumour removal. In contrast, age within this older group, general fitness before surgery, the presence of other medical conditions, tumour size, and molecular tumour features did not show a clear link with survival. Notably, a history of smoking was associated with poorer survival, even after accounting for other factors. Taken together, these findings suggest that selected patients aged 70 and over can still benefit from active, combined treatment approaches, and that early, coordinated decision-making around surgery and post-operative therapy is important to maximise potential survival benefits in this growing patient group.

</li>
<li>Keywords: glioblastoma; older patients; surgical resection; adjuvant chemoradiotherapy</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E5   |  10 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/178'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Ali, A.M.S.; Parmar, V.; Hannan, C.J.; Farah, J.O. Predictors of Survival in Patients Aged ≥70 with Glioblastoma: A Time-Dependent Multivariable Analysis. Cancers 2026, 18, 178. https://doi.org/10.3390/cancers18010178<br>
Type: Article  |  Publication date: 05 January 2026<br>
<br>
</li>
<li>Summary: Glioblastoma is an aggressive brain tumour with a very poor outlook, particularly in older patients, and its incidence is expected to rise as the population ages. This study reviewed the outcomes of 124 patients aged 70 years or older who underwent surgery for glioblastoma at a single specialist neurosurgical centre between 2021 and 2025, with the aim of identifying factors linked to survival. Overall survival remained limited, with a median survival of around 8 months. Two factors were clearly associated with longer survival. Patients who received chemotherapy and radiotherapy after surgery lived longer than those who did not, with the benefit being strongest in the early months following surgery and gradually reducing over time. In addition, patients in whom all visible tumour could be removed during surgery tended to live longer than those who had only partial tumour removal. In contrast, age within this older group, general fitness before surgery, the presence of other medical conditions, tumour size, and molecular tumour features did not show a clear link with survival. Notably, a history of smoking was associated with poorer survival, even after accounting for other factors. Taken together, these findings suggest that selected patients aged 70 and over can still benefit from active, combined treatment approaches, and that early, coordinated decision-making around surgery and post-operative therapy is important to maximise potential survival benefits in this growing patient group.<br>
<br>
</li>
<li>Keywords: glioblastoma; older patients; surgical resection; adjuvant chemoradiotherapy</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/yqfjepw722cnvv5r/E5_-_Glioblastoma_Survival_in_Elderly.mp3" length="13526247" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E5   |  10 min   |   Latest   |  Publication Link

Podcast based on: Ali, A.M.S.; Parmar, V.; Hannan, C.J.; Farah, J.O. Predictors of Survival in Patients Aged ≥70 with Glioblastoma: A Time-Dependent Multivariable Analysis. Cancers 2026, 18, 178. https://doi.org/10.3390/cancers18010178Type: Article  |  Publication date: 05 January 2026
Summary: Glioblastoma is an aggressive brain tumour with a very poor outlook, particularly in older patients, and its incidence is expected to rise as the population ages. This study reviewed the outcomes of 124 patients aged 70 years or older who underwent surgery for glioblastoma at a single specialist neurosurgical centre between 2021 and 2025, with the aim of identifying factors linked to survival. Overall survival remained limited, with a median survival of around 8 months. Two factors were clearly associated with longer survival. Patients who received chemotherapy and radiotherapy after surgery lived longer than those who did not, with the benefit being strongest in the early months following surgery and gradually reducing over time. In addition, patients in whom all visible tumour could be removed during surgery tended to live longer than those who had only partial tumour removal. In contrast, age within this older group, general fitness before surgery, the presence of other medical conditions, tumour size, and molecular tumour features did not show a clear link with survival. Notably, a history of smoking was associated with poorer survival, even after accounting for other factors. Taken together, these findings suggest that selected patients aged 70 and over can still benefit from active, combined treatment approaches, and that early, coordinated decision-making around surgery and post-operative therapy is important to maximise potential survival benefits in this growing patient group.
Keywords: glioblastoma; older patients; surgical resection; adjuvant chemoradiotherapy

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>563</itunes:duration>
                <itunes:episode>5</itunes:episode>
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            </item>
    <item>
        <title>E4 - Imaging in Ovarian Cancer</title>
        <itunes:title>E4 - Imaging in Ovarian Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e4-imaging-in-ovarian-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e4-imaging-in-ovarian-cancer/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:30:17 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/d3ea117e-44b7-3e05-9217-5db3bdf36d99</guid>
                                    <description><![CDATA[<p>E4   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/173'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: D’Amario, A.; Ambrosini, R.; Gullino, A.; Grazioli, L. Role of Imaging Techniques in Ovarian Cancer Diagnosis: Current Approaches and Future Directions. Cancers 2026, 18, 173. https://doi.org/10.3390/cancers18010173
Type: Review  |  Publication date: 04 January 2026

</li>
<li>Summary: Ovarian cancer is a leading cause of death among gynecological malignancies. Standard ultrasound scans may not be conclusive, especially when ovarian masses are difficult to classify. This review highlights recent advances aimed at reducing diagnostic uncertainty. Contrast-enhanced MRI has demonstrated high accuracy in differentiating benign from malignant lesions, and the O-RADS MRI scoring system provides structured risk assessment with strong sensitivity and specificity. New classification methods are also being developed to further support clinical decision-making. In addition, artificial intelligence (AI) approaches, including machine learning and deep learning, are being tested to improve diagnostic precision by analyzing complex imaging data. Overall, the integration of advanced imaging with AI has the potential to substantially improve the evaluation and management of women with suspected ovarian cancer.

</li>
<li>Keywords: ovarian cancer; Ultrasound (US); Computed Tomography (CT); Magnetic Resonance Imaging (MRI); O-RADS MRI Score; Artificial Intelligence (AI); radiomics</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E4   |  14 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/173'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: D’Amario, A.; Ambrosini, R.; Gullino, A.; Grazioli, L. Role of Imaging Techniques in Ovarian Cancer Diagnosis: Current Approaches and Future Directions. Cancers 2026, 18, 173. https://doi.org/10.3390/cancers18010173<br>
Type: Review  |  Publication date: 04 January 2026<br>
<br>
</li>
<li>Summary: Ovarian cancer is a leading cause of death among gynecological malignancies. Standard ultrasound scans may not be conclusive, especially when ovarian masses are difficult to classify. This review highlights recent advances aimed at reducing diagnostic uncertainty. Contrast-enhanced MRI has demonstrated high accuracy in differentiating benign from malignant lesions, and the O-RADS MRI scoring system provides structured risk assessment with strong sensitivity and specificity. New classification methods are also being developed to further support clinical decision-making. In addition, artificial intelligence (AI) approaches, including machine learning and deep learning, are being tested to improve diagnostic precision by analyzing complex imaging data. Overall, the integration of advanced imaging with AI has the potential to substantially improve the evaluation and management of women with suspected ovarian cancer.<br>
<br>
</li>
<li>Keywords: ovarian cancer; Ultrasound (US); Computed Tomography (CT); Magnetic Resonance Imaging (MRI); O-RADS MRI Score; Artificial Intelligence (AI); radiomics</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/j9p5ax5ih3kc8et4/E4_-_Imaging_in_Ovarian_Cancer.mp3" length="19227628" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E4   |  14 min   |   Latest   |  Publication Link

Podcast based on: D’Amario, A.; Ambrosini, R.; Gullino, A.; Grazioli, L. Role of Imaging Techniques in Ovarian Cancer Diagnosis: Current Approaches and Future Directions. Cancers 2026, 18, 173. https://doi.org/10.3390/cancers18010173Type: Review  |  Publication date: 04 January 2026
Summary: Ovarian cancer is a leading cause of death among gynecological malignancies. Standard ultrasound scans may not be conclusive, especially when ovarian masses are difficult to classify. This review highlights recent advances aimed at reducing diagnostic uncertainty. Contrast-enhanced MRI has demonstrated high accuracy in differentiating benign from malignant lesions, and the O-RADS MRI scoring system provides structured risk assessment with strong sensitivity and specificity. New classification methods are also being developed to further support clinical decision-making. In addition, artificial intelligence (AI) approaches, including machine learning and deep learning, are being tested to improve diagnostic precision by analyzing complex imaging data. Overall, the integration of advanced imaging with AI has the potential to substantially improve the evaluation and management of women with suspected ovarian cancer.
Keywords: ovarian cancer; Ultrasound (US); Computed Tomography (CT); Magnetic Resonance Imaging (MRI); O-RADS MRI Score; Artificial Intelligence (AI); radiomics

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>801</itunes:duration>
                <itunes:episode>4</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E3 - APOBEC3C in Prostate Cancer</title>
        <itunes:title>E3 - APOBEC3C in Prostate Cancer</itunes:title>
        <link>https://podcast.sinapsos.com/e/e3-apobec3c-in-prostate-cancer/</link>
                    <comments>https://podcast.sinapsos.com/e/e3-apobec3c-in-prostate-cancer/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:29:38 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/7ff6741f-7fdd-33d2-8120-459c8d7eba84</guid>
                                    <description><![CDATA[<p>E3   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/170'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Pang, Z.; Wang, J.; Xu, Y.; Ji, B.; Ren, M.; Ding, B. APOBEC3C Suppresses Prostate Cancer by Regulating Key Molecules Involved in Cellular Inflammation, Cell Cycle Arrest, and DNA Damage Response. Cancers 2026, 18, 170. https://doi.org/10.3390/cancers18010170
Type: Article  |  Publication date: 03 January 2026

</li>
<li>Summary: Given the clinical challenge of advanced, therapy-resistant prostate cancer (PCa), this study aimed to identify novel molecular drivers. Using transcriptomic data from the TCGA and GEO databases, combined with WGCNA, differential expression analysis, and LASSO regression, APOBEC3C (A3C) was identified as a key candidate, whose downregulation in PCa tumors correlated with advanced T stage, higher Gleason scores, and poor survival. Bioinformatic analysis linked high A3C expression to an anti-tumor immune microenvironment (e.g., increased CD8+ T cell infiltration and reduced M2 macrophages). In vitro assays confirmed that A3C overexpression suppressed PCa cell proliferation, migration, and invasion, while its knockdown promoted these malignant phenotypes. Mechanistically, A3C enhances the expression levels of STING1 and its downstream molecules, including Caspase1, IL-18, and IL-1β, upregulating DNA damage protective genes (GSTP1 and GPX3) and enhancing cell cycle regulator GAS1 expression. Collectively, this study establishes A3C as a PCa suppressor that impedes tumor progression via multiple key pathways.

</li>
<li>Keywords: APOBEC3C; prostate cancer; prognosis; immune microenvironment; inflammation</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E3   |  11 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/170'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Pang, Z.; Wang, J.; Xu, Y.; Ji, B.; Ren, M.; Ding, B. APOBEC3C Suppresses Prostate Cancer by Regulating Key Molecules Involved in Cellular Inflammation, Cell Cycle Arrest, and DNA Damage Response. Cancers 2026, 18, 170. https://doi.org/10.3390/cancers18010170<br>
Type: Article  |  Publication date: 03 January 2026<br>
<br>
</li>
<li>Summary: Given the clinical challenge of advanced, therapy-resistant prostate cancer (PCa), this study aimed to identify novel molecular drivers. Using transcriptomic data from the TCGA and GEO databases, combined with WGCNA, differential expression analysis, and LASSO regression, APOBEC3C (A3C) was identified as a key candidate, whose downregulation in PCa tumors correlated with advanced T stage, higher Gleason scores, and poor survival. Bioinformatic analysis linked high A3C expression to an anti-tumor immune microenvironment (e.g., increased CD8+ T cell infiltration and reduced M2 macrophages). In vitro assays confirmed that A3C overexpression suppressed PCa cell proliferation, migration, and invasion, while its knockdown promoted these malignant phenotypes. Mechanistically, A3C enhances the expression levels of STING1 and its downstream molecules, including Caspase1, IL-18, and IL-1β, upregulating DNA damage protective genes (GSTP1 and GPX3) and enhancing cell cycle regulator GAS1 expression. Collectively, this study establishes A3C as a PCa suppressor that impedes tumor progression via multiple key pathways.<br>
<br>
</li>
<li>Keywords: APOBEC3C; prostate cancer; prognosis; immune microenvironment; inflammation</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/p97i3mmg6hbvi94a/E3_-_APOBEC3C_in_Prostate_Cancer.mp3" length="14897989" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E3   |  11 min   |   Latest   |  Publication Link

Podcast based on: Pang, Z.; Wang, J.; Xu, Y.; Ji, B.; Ren, M.; Ding, B. APOBEC3C Suppresses Prostate Cancer by Regulating Key Molecules Involved in Cellular Inflammation, Cell Cycle Arrest, and DNA Damage Response. Cancers 2026, 18, 170. https://doi.org/10.3390/cancers18010170Type: Article  |  Publication date: 03 January 2026
Summary: Given the clinical challenge of advanced, therapy-resistant prostate cancer (PCa), this study aimed to identify novel molecular drivers. Using transcriptomic data from the TCGA and GEO databases, combined with WGCNA, differential expression analysis, and LASSO regression, APOBEC3C (A3C) was identified as a key candidate, whose downregulation in PCa tumors correlated with advanced T stage, higher Gleason scores, and poor survival. Bioinformatic analysis linked high A3C expression to an anti-tumor immune microenvironment (e.g., increased CD8+ T cell infiltration and reduced M2 macrophages). In vitro assays confirmed that A3C overexpression suppressed PCa cell proliferation, migration, and invasion, while its knockdown promoted these malignant phenotypes. Mechanistically, A3C enhances the expression levels of STING1 and its downstream molecules, including Caspase1, IL-18, and IL-1β, upregulating DNA damage protective genes (GSTP1 and GPX3) and enhancing cell cycle regulator GAS1 expression. Collectively, this study establishes A3C as a PCa suppressor that impedes tumor progression via multiple key pathways.
Keywords: APOBEC3C; prostate cancer; prognosis; immune microenvironment; inflammation

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
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        <itunes:block>No</itunes:block>
        <itunes:duration>620</itunes:duration>
                <itunes:episode>3</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
            </item>
    <item>
        <title>E2 - Intracranial SRT Cost-Effectiveness</title>
        <itunes:title>E2 - Intracranial SRT Cost-Effectiveness</itunes:title>
        <link>https://podcast.sinapsos.com/e/e2-intracranial-srt-costeffectiveness/</link>
                    <comments>https://podcast.sinapsos.com/e/e2-intracranial-srt-costeffectiveness/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:28:58 +0000</pubDate>
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                                    <description><![CDATA[<p>E2   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/163'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Zhang, Q.; Gao, L.; Das, N.; Squire, T.; Stoker, D.; Shakya, R.; Patel, D.; Joshi, A.; Xing, T. Cost-Effectiveness Analysis of an Intracranial Stereotactic Radiotherapy Service for Brain Metastasis in a North Queensland Regional Cancer Centre. Cancers 2026, 18, 163. https://doi.org/10.3390/cancers18010163
Type: Article  |  Publication date: 02 January 2026

</li>
<li>Summary: Rural and regional Australian patients, especially Aboriginal and Torres Strait Islander patients, are faced with multifaceted challenges when receiving a referral to metropolitan centres for specialist medical care, which affects the uptake of recommended treatment and therefore negatively impacts the outcome. Being able to access specialist care closer to home improves the accessibility and timeliness of recommended treatment. To the best of our knowledge, this is the first study reporting the cost-effectiveness of the implementation of an intracranial SRS service at an Australian regional cancer centre. This study provides evidence to initiate further discussions on the identification of suitable cancer care models to deliver specialist care from funding and policy support perspectives.

</li>
<li>Keywords: stereotactic radiosurgery; brain metastasis; health economy; radiotherapy</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E2   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/163'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Zhang, Q.; Gao, L.; Das, N.; Squire, T.; Stoker, D.; Shakya, R.; Patel, D.; Joshi, A.; Xing, T. Cost-Effectiveness Analysis of an Intracranial Stereotactic Radiotherapy Service for Brain Metastasis in a North Queensland Regional Cancer Centre. Cancers 2026, 18, 163. https://doi.org/10.3390/cancers18010163<br>
Type: Article  |  Publication date: 02 January 2026<br>
<br>
</li>
<li>Summary: Rural and regional Australian patients, especially Aboriginal and Torres Strait Islander patients, are faced with multifaceted challenges when receiving a referral to metropolitan centres for specialist medical care, which affects the uptake of recommended treatment and therefore negatively impacts the outcome. Being able to access specialist care closer to home improves the accessibility and timeliness of recommended treatment. To the best of our knowledge, this is the first study reporting the cost-effectiveness of the implementation of an intracranial SRS service at an Australian regional cancer centre. This study provides evidence to initiate further discussions on the identification of suitable cancer care models to deliver specialist care from funding and policy support perspectives.<br>
<br>
</li>
<li>Keywords: stereotactic radiosurgery; brain metastasis; health economy; radiotherapy</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/8ghmpxr3fajqvg3i/E2_-_Intracranial_SRT_CostEffectiveness.mp3" length="15934945" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E2   |  12 min   |   Latest   |  Publication Link

Podcast based on: Zhang, Q.; Gao, L.; Das, N.; Squire, T.; Stoker, D.; Shakya, R.; Patel, D.; Joshi, A.; Xing, T. Cost-Effectiveness Analysis of an Intracranial Stereotactic Radiotherapy Service for Brain Metastasis in a North Queensland Regional Cancer Centre. Cancers 2026, 18, 163. https://doi.org/10.3390/cancers18010163Type: Article  |  Publication date: 02 January 2026
Summary: Rural and regional Australian patients, especially Aboriginal and Torres Strait Islander patients, are faced with multifaceted challenges when receiving a referral to metropolitan centres for specialist medical care, which affects the uptake of recommended treatment and therefore negatively impacts the outcome. Being able to access specialist care closer to home improves the accessibility and timeliness of recommended treatment. To the best of our knowledge, this is the first study reporting the cost-effectiveness of the implementation of an intracranial SRS service at an Australian regional cancer centre. This study provides evidence to initiate further discussions on the identification of suitable cancer care models to deliver specialist care from funding and policy support perspectives.
Keywords: stereotactic radiosurgery; brain metastasis; health economy; radiotherapy

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>663</itunes:duration>
                <itunes:episode>2</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
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    <item>
        <title>E1 - Esophageal Cancer Neoadjuvant Comparison</title>
        <itunes:title>E1 - Esophageal Cancer Neoadjuvant Comparison</itunes:title>
        <link>https://podcast.sinapsos.com/e/e1-esophageal-cancer-neoadjuvant-comparison/</link>
                    <comments>https://podcast.sinapsos.com/e/e1-esophageal-cancer-neoadjuvant-comparison/#comments</comments>        <pubDate>Sun, 11 Jan 2026 20:28:19 +0000</pubDate>
        <guid isPermaLink="false">sinapsospodcast-oncology.podbean.com/e7ed870a-be83-3c64-b38a-5dd3a1a57401</guid>
                                    <description><![CDATA[<p>E1   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/155'>Publication Link</a>
</p>
<ul>
<li>Podcast based on: Deng, S.; Yan, X.; Peng, Y.; Zhu, L.; Shen, Y.; Ying, W.; Xu, Y.; Fu, Z. Three-Year Outcomes of Neoadjuvant Chemoimmunotherapy vs. Neoadjuvant Chemoradiotherapy in Resectable Esophageal Cancer: A Multicenter Retrospective Study. Cancers 2026, 18, 155. https://doi.org/10.3390/cancers18010155
Type: Article  |  Publication date: 01 January 2026

</li>
<li>Summary: Evidence regarding neoadjuvant chemoimmunotherapy (nCIT) or neoadjuvant chemoradiotherapy (nCRT) for resectable locally advanced esophageal squamous cell carcinoma (LA-ESCC) remains controversial. This study (n = 225) investigated the long-term efficacy and safety of nCIT versus nCRT in patients with LA-ESCC. The results suggest that nCIT can improve the long-term survival of patients with resectable esophageal cancer, whereas nCRT may provide greater benefits in patients with node-positive (N+) or non-cT4-stage disease. This study demonstrates the clinical efficacy and safety of nCIT in patients with LA-ESCC.

</li>
<li>Keywords: locally advanced resectable esophageal squamous cell carcinoma; neoadjuvant chemoradiotherapy; immunotherapy; survival</li>
</ul>
<p> </p>
<p>License and disclaimer:
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></description>
                                                            <content:encoded><![CDATA[<p>E1   |  12 min   |   Latest   |  <a href='https://www.mdpi.com/2072-6694/18/1/155'>Publication Link</a><br>
</p>
<ul>
<li>Podcast based on: Deng, S.; Yan, X.; Peng, Y.; Zhu, L.; Shen, Y.; Ying, W.; Xu, Y.; Fu, Z. Three-Year Outcomes of Neoadjuvant Chemoimmunotherapy vs. Neoadjuvant Chemoradiotherapy in Resectable Esophageal Cancer: A Multicenter Retrospective Study. Cancers 2026, 18, 155. https://doi.org/10.3390/cancers18010155<br>
Type: Article  |  Publication date: 01 January 2026<br>
<br>
</li>
<li>Summary: Evidence regarding neoadjuvant chemoimmunotherapy (nCIT) or neoadjuvant chemoradiotherapy (nCRT) for resectable locally advanced esophageal squamous cell carcinoma (LA-ESCC) remains controversial. This study (n = 225) investigated the long-term efficacy and safety of nCIT versus nCRT in patients with LA-ESCC. The results suggest that nCIT can improve the long-term survival of patients with resectable esophageal cancer, whereas nCRT may provide greater benefits in patients with node-positive (N+) or non-cT4-stage disease. This study demonstrates the clinical efficacy and safety of nCIT in patients with LA-ESCC.<br>
<br>
</li>
<li>Keywords: locally advanced resectable esophageal squamous cell carcinoma; neoadjuvant chemoradiotherapy; immunotherapy; survival</li>
</ul>
<p> </p>
<p>License and disclaimer:<br>
Original article © 2026 by the authors. Licensed under the <a href='https://creativecommons.org/licenses/by/4.0/'>Creative Commons Attribution 4.0 (CC BY 4.0)</a> license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.</p>
<p> </p>
]]></content:encoded>
                                    
        <enclosure url="https://mcdn.podbean.com/mf/web/bvzzwzv5pcfwtke9/E1_-_Esophageal_Cancer_Neoadjuvant_Comparison.mp3" length="16937421" type="audio/mpeg"/>
        <itunes:summary><![CDATA[E1   |  12 min   |   Latest   |  Publication Link

Podcast based on: Deng, S.; Yan, X.; Peng, Y.; Zhu, L.; Shen, Y.; Ying, W.; Xu, Y.; Fu, Z. Three-Year Outcomes of Neoadjuvant Chemoimmunotherapy vs. Neoadjuvant Chemoradiotherapy in Resectable Esophageal Cancer: A Multicenter Retrospective Study. Cancers 2026, 18, 155. https://doi.org/10.3390/cancers18010155Type: Article  |  Publication date: 01 January 2026
Summary: Evidence regarding neoadjuvant chemoimmunotherapy (nCIT) or neoadjuvant chemoradiotherapy (nCRT) for resectable locally advanced esophageal squamous cell carcinoma (LA-ESCC) remains controversial. This study (n = 225) investigated the long-term efficacy and safety of nCIT versus nCRT in patients with LA-ESCC. The results suggest that nCIT can improve the long-term survival of patients with resectable esophageal cancer, whereas nCRT may provide greater benefits in patients with node-positive (N+) or non-cT4-stage disease. This study demonstrates the clinical efficacy and safety of nCIT in patients with LA-ESCC.
Keywords: locally advanced resectable esophageal squamous cell carcinoma; neoadjuvant chemoradiotherapy; immunotherapy; survival

 
License and disclaimer:Original article © 2026 by the authors. Licensed under the Creative Commons Attribution 4.0 (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). This episode is an AI-generated audio adaptation of the article: the script and the voices are synthetic, changes were made, and the adaptation is not endorsed by the authors, the journal, or the publisher. It may contain errors or omissions, so consult the original publication before relying on any detail. It is for educational purposes only and is not medical advice. The creators accept no liability for any use of this content.
 ]]></itunes:summary>
        <itunes:author>Sinapsos Podcast</itunes:author>
        <itunes:explicit>false</itunes:explicit>
        <itunes:block>No</itunes:block>
        <itunes:duration>705</itunes:duration>
        <itunes:season>1</itunes:season>
        <itunes:episode>1</itunes:episode>
        <itunes:episodeType>full</itunes:episodeType>
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