Podcasts about tkis

Play Episode Listen Later Jul 16, 2026 15:58

Please visit answersincme.com/TNM860 to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Richard Kim, MD. In this activity, an expert in oncology discusses when and how to sequence later-line and chemotherapy-free therapies in metastatic colorectal cancer (mCRC). Upon completion of this activity, participants should be better able to: Evaluate factors influencing a treatment switch from cytotoxic agents for patients with stable metastatic colorectal cancer (mCRC); Formulate practical approaches for transitioning from chemotherapy to tyrosine kinase inhibitor (TKI) treatment in later-line settings for patients with mCRC; and Describe strategies to prolong chemotherapy-free disease control with TKIs.

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S17 Ep45: Medical Crossfire®: Precision Oncology in NSCLC – Translating HER2 and TROP2 Innovation into Practice-Changing Care

Oncology Peer Review On-The-Go

Play Episode Listen Later Jul 7, 2026 32:18

Highlights from the PER® CME activity "Medical Crossfire®: Precision Oncology in NSCLC – Translating HER2 and TROP2 Innovation into Practice-Changing Care" — this podcast is not certified for credit. To participate in the full accredited activity and earn CME credit, use the link below.In this podcast, focusing on precision oncology in non-small cell lung cancer (NSCLC), experts Helena Yu, MD; Jacob Sands, MD; and Sarah Goldberg MD, MPH; will discuss the rapidly evolving landscape of Human Epidermal growth factor Receptor 2 (HER2)- and Trophoblast cell-surface antigen 2 (TROP2)-directed therapies in NSCLC. The podcast covers the spectrum of targeted agents from antibody-drug conjugates (ADCs) to novel HER2-selective tyrosine kinase inhibitors (TKIs), along with key clinical trial data and practical strategies for managing the unique adverse event profiles associated with these treatments.Earn CME credit by completing the full accredited activity (available through June 30, 2027): https://www.gotoper.com/courses/medical-crossfire-precision-oncology-in-nsclc-translating-her2-and-trop2-innovation-into-practice-changing-care-mr5qThis podcast, including the narration, was developed by PER® (Physicians' Education Resource®, LLC) editorial staff from the full online CME activity developed with these faculty. The narration was voiced by a PER staff member or by an AI tool. The podcast contains no product advertising. The full activity is supported by educational grants from AstraZeneca Pharmaceuticals; Daiichi Sankyo, Inc.; and Gilead Sciences, Inc.This content is for educational purposes only and is not a substitute for the independent clinical judgment of a health care professional. Faculty may discuss investigational or off-label uses; consult prescribing information for any products discussed.

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S1 Ep223: Optimizing Frontline Selection and Treatment-Free Remission in CML

Play Episode Listen Later Jul 1, 2026 34:28

Experts discuss the evolving frontline CML treatment landscape, the impact of asciminib, and clinical strategies for achieving treatment-free remission.Once considered a terminal diagnosis, chronic myeloid leukemia (CML) in chronic phase has been fundamentally rewritten as a highly manageable chronic condition. In this episode of Oncology on the Go, Joshua Zeidner, MD, and Jorge E. Cortes, MD, sat down to explore the rapidly shifting therapeutic paradigm of frontline CML management. The discussion tracked the monumental evolution of treatment from early bone marrow transplants to the introduction of imatinib (Gleevec) and subsequent generations of tyrosine kinase inhibitors (TKIs). The experts dove deep into the practice-changing data from the phase 3 ASC4FIRST trial (NCT04971226), analyzing how the newly introduced STAMP inhibitor, asciminib (Scemblix), is challenging traditional treatment sequencing due to its superior efficacy and highly favorable toxicity profile.In the ASC4FIRST trial, the major molecular response (MMR) rate was 74.1% with asciminib vs 52.0% with other investigator-selected TKIs. The MMR rate at week 96 was consistently higher with asciminib vs other investigator-selected TKIs and imatinib across all assessed demographic and prognostic subgroups. Overall, investigators concluded that asciminib demonstrated a favorable risk-benefit profile compared with other standard therapies and presented a “valuable frontline option” for patients with CML in chronic phase.Zeidner and Cortes also shared practical clinical insights on: Shared Decision-Making: Tailoring frontline selections based on patient lifestyle, comorbidities, and preferences. Navigating Milestones: Balancing strict NCCN/European LeukemiaNet molecular response guidelines with individualized, real-world context. The Art of Discontinuation: Using strategic timing and criteria (such as achieving sustained MR4.5) to optimize success rates for treatment-free remission. The Next Frontier: Managing resistance mutations and mapping out second- and third-line therapies in an evolving post-asciminib landscape. Zeider is professor of medicine, chief of Leukemia Research, and director of Clinical Cancer Research Commercial Integration at the University of North Caroline-Chapel Hill Cancer Therapeutics Research Program. Cortes is associate director for Translation at the University of Alabama O'Neal Cancer Center. To watch the full discussion, visit: https://www.cancernetwork.com/between-the-lines/oncology-on-the-go-frontline-chronic-myeloid-leukemia-in-chronic-phase-optimizing-treatmentReferenceCortes JE, Hughes TP, Wang J, et al. Asciminib demonstrates superior efficacy and safety in newly diagnosed chronic myeloid leukemia in the ASC4FIRST trial. Blood. 2026;147(3):1433-1446. doi:10.1182/blood.2025029210

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Personalizing EGFR Mutation–Positive NSCLC Care: Strategies for the Advanced Practice Provider

CCO Oncology Podcast

Play Episode Listen Later Jun 22, 2026 26:58

Link to claim CME credit: https://bit.ly/4uRr3ir In this episode, Elizabeth Krueger, NP, and Sam Vafadar, DHSc, PA-C, discuss how they optimize first-line EGFR-targeted therapy for patients with EGFR-mutated NSCLC, including: First-line treatment options available for EGFR-mutated NSCLC and the clinical trials that resulted in their approval Adverse event identification and management Generalized strategies to support patient adherence to TKIs Get access to all of our new podcasts by subscribing to the Decera Clinical Education Podcast on Apple Podcasts, YouTube Music, or Spotify Presenters: Elizabeth Krueger, NP Center for Thoracic Cancers Mass General Brigham Cancer Institute Boston, Massachusetts Sam Vafadar, DHSc, PA-C Physician Associate Department of Thoracic Oncology H. Lee Moffitt Cancer Center and Research Institute Tampa, Florida Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

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To hold or NOT to hold Systemic Therapy with Radiation: Dr. Nina Sanford

New Retina Radio by Eyetube

Play Episode Listen Later Jun 18, 2026 23:56

Welcome back to the Oncology Brothers podcast! In this episode, we were joined by Dr. Nina Sanford, a GI radiation oncologist from UT Southwestern, to discuss a critical topic in cancer treatment: when to hold and not to hold systemic therapy during radiation and for how long. Join us as we explore: The framework for balancing systemic therapy with different types of radiation, including SBRT, palliative, and conventional radiation. Insights on managing cytotoxic chemotherapy, immunotherapy, TKIs, and targeted therapies in conjunction with radiation. The importance of individualized treatment plans and the evolving data around various drug classes, including BRAF inhibitors, PARP inhibitors, and anti-HER2 therapies. Practical recommendations for community oncologists navigating these complex decisions. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Don't forget to check out Dr. Sanford's teaching video for more in-depth information! #RadiationOncology, #SystemicTherapy, #SBRT, #MultidisciplinaryCare, #OncologyBrothers

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ARVO '26: TKIs for Wet AMD and How We Got to the AI Era of Research

Play Episode Listen Later Jun 18, 2026 32:48

TKIs are all the rage. But what do the data tell us about their ability to effectively treat wet AMD? Akshay Thomas, MD, outlines findings from DAVIO 2, the phase 2 study assessing the safety and efficacy of EYP-1901 (EyePoint Pharmaceuticals) for the treatment of wet AMD. And Aaron Lee, MD, MSCI, and Cecelia Lee, MD, MS, recap their Cogan Award Lecture from this year's ARVO annual meeting. Hear how they envision a future of ophthalmic research driven by AI and machine learning—and how they know we can only get there by looking back at where we've been.

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Beyond the Biomarker: Bridging Patient Voices and Precision Care in HER2-Mutant NSCLC

CME in Minutes: Education in Rheumatology, Immunology, & Infectious Diseases

Play Episode Listen Later Jun 11, 2026 19:11

Please visit answersincme.com/CNW860 to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Stephen V. Liu, MD and Amber Fake. In this activity, an expert in non–small-cell lung cancer (NSCLC) discusses the evolving patient-centered management of HER2-mutant NSCLC, focusing on the use of HER2-targeted TKIs. Upon completion of this activity, participants should be better able to: Describe how HER2-targeted TKIs may address the clinical needs for diverse patient populations with HER2-mutant NSCLC; Implement evidence-based molecular profiling to identify HER2 alterations in NSCLC; Evaluate the clinical evidence of current and emerging HER2-targeted treatments; and Integrate shared decision-making strategies to align preferences for patients with HER2-mutant NSCLC.

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Beyond the Biomarker: Bridging Patient Voices and Precision Care in HER2-Mutant NSCLC

Play Episode Listen Later Jun 11, 2026 19:11

Please visit answersincme.com/CNW860 to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Stephen V. Liu, MD and Amber Fake. In this activity, an expert in non–small-cell lung cancer (NSCLC) discusses the evolving patient-centered management of HER2-mutant NSCLC, focusing on the use of HER2-targeted TKIs. Upon completion of this activity, participants should be better able to: Describe how HER2-targeted TKIs may address the clinical needs for diverse patient populations with HER2-mutant NSCLC; Implement evidence-based molecular profiling to identify HER2 alterations in NSCLC; Evaluate the clinical evidence of current and emerging HER2-targeted treatments; and Integrate shared decision-making strategies to align preferences for patients with HER2-mutant NSCLC.

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The Promise of Oral Therapy for HER2-Mutated NSCLC: Unlocking New Treatment Opportunities With a Familiar Target

Play Episode Listen Later Jun 5, 2026 73:30

Please visit answersincme.com/860/IME_2025_00012595-replay to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by John V. Heymach, MD, PhD; and Mark Awad, MD, PhD. In this activity, experts in oncology discuss the role of dual and HER2-selective oral tyrosine kinase inhibitors in patients with HER2-mutated non–small-cell lung cancer. Upon completion of this activity, participants should be better able to: Specify how TKIs may address unmet therapeutic needs for diverse patient populations with HER2-mutated NSCLC; Interpret the clinical evidence for approved oral TKIs for patients with HER2-mutated NSCLC; and Assess which patients may be candidates for approved oral HER2-targeting TKIs in the context of the current standard of care.

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S17 Ep25: TKIs Continue to Move Forward and Expand Their Potential in CML: With Michael J. Mauro, MD

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Play Episode Listen Later May 23, 2026 16:59

In today's episode, we spoke with Michael J. Mauro, MD, an attending physician at Memorial Sloan Kettering Cancer Center in New York, New York.In our exclusive interview, Dr Mauro discussed the vast assortment of TKIs available for the treatment of patients with chronic myeloid leukemia (CML). In addition to breaking down numerous different TKIs that he turns to in clinical practice and their accompanying data, Mauro also dissected the November 2025 FDA approval of generic dasatinib (Phyrago) tablets for patients with CML and acute lymphoblastic leukemia. More specifically, Mauro outlined what this approval means for patients who need concomitant gastric acid–reducing agents like proton pump inhibitors.

Challenging Cases in Chronic Myeloid Leukemia (CML): Drs. Fadi Haddad & Gaby Hobbs

CME in Minutes: Education in Rheumatology, Immunology, & Infectious Diseases

Play Episode Listen Later May 22, 2026 21:50

Welcome to the Oncology Brothers podcast! In this episode, we dived into the complexities of chronic myeloid leukemia (CML) through two challenging case studies. Joined by CML experts Dr. Fadi Haddad from MD Anderson Cancer Center and Dr. Gaby Hobbs from Massachusetts General Hospital, Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers ⁠Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ we talked about: The initial workup for diagnosing CML, including the importance of CBC, bone marrow biopsy, and BCR-ABL testing. How to select the most optimal frontline treatment option amongst many available, considering factors like age, comorbidities, and the goal of treatment-free remission (TFR). The role of first-generation TKI, but also how newer TKIs assist in achieving deeper molecular remissions. Strategies for managing treatment breaks and monitoring patients in remission. The role of ponatinib as a pan-BCR:ABL1 inhibitor effective against all known resistance mutations, including T315I, and the optimized response-based dosing strategy to balance efficacy with safety. Tune in for valuable insights on treatment strategies, patient management, and the latest advancements in CML care. Don't forget to like, subscribe, and share your challenging case scenarios for future discussions! #ChronicMyeloidLeukemia, #CML, #TreatmentFreeRemission, #OncologyBrothers

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From Burden to Breakthrough: The Rise of KIT D816V-Selective Therapy in Indolent Systemic Mastocytosis

Play Episode Listen Later May 5, 2026 14:12

Please visit answersincme.com/ZTY860 to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Daniel J. DeAngelo, MD, PhD. In this activity, an expert in hematology discusses targeted treatment options for the management of indolent systemic mastocytosis. Upon completion of this activity, participants should be better able to: Recognize the impacts of indolent systemic mastocytosis (ISM) on patients' quality of life; Discuss the clinical significance of selective KIT D816V–targeting tyrosine kinase inhibitors (TKIs) in the management of patients with ISM; and Design patient-centered strategies for integrating selective KIT D816V–targeting TKIs into the management of ISM.

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From Burden to Breakthrough: The Rise of KIT D816V-Selective Therapy in Indolent Systemic Mastocytosis

CME in Minutes: Education in Dermatology

Play Episode Listen Later May 5, 2026 14:12

Please visit answersincme.com/ZTY860 to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Daniel J. DeAngelo, MD, PhD. In this activity, an expert in hematology discusses targeted treatment options for the management of indolent systemic mastocytosis. Upon completion of this activity, participants should be better able to: Recognize the impacts of indolent systemic mastocytosis (ISM) on patients' quality of life; Discuss the clinical significance of selective KIT D816V–targeting tyrosine kinase inhibitors (TKIs) in the management of patients with ISM; and Design patient-centered strategies for integrating selective KIT D816V–targeting TKIs into the management of ISM.

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From Burden to Breakthrough: The Rise of KIT D816V-Selective Therapy in Indolent Systemic Mastocytosis

Play Episode Listen Later May 5, 2026 14:12

Please visit answersincme.com/ZTY860 to participate, download slides and supporting materials, complete the post test, and get a certificate. Presented by Daniel J. DeAngelo, MD, PhD. In this activity, an expert in hematology discusses targeted treatment options for the management of indolent systemic mastocytosis. Upon completion of this activity, participants should be better able to: Recognize the impacts of indolent systemic mastocytosis (ISM) on patients' quality of life; Discuss the clinical significance of selective KIT D816V–targeting tyrosine kinase inhibitors (TKIs) in the management of patients with ISM; and Design patient-centered strategies for integrating selective KIT D816V–targeting TKIs into the management of ISM.

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The PBS Update April 2026: Expanded Indications + New Rare Cancer Options

The Oncology Podcast

Play Episode Listen Later Apr 15, 2026 20:22 Transcription Available

Send us Fan MailProudly Produced by The Oncology NetworkProfessor Craig Underhill and Rachael Babin break down the key oncology changes from the April 2026 PBS update.This month we run through six fresh PBS listings and policy changes that affect Australian oncology and haematology practice, from ROS1-positive non small cell lung cancer to perioperative immunotherapy and late-line blood cancer options. We focus on who benefits, what the key trial signals are and what clinicians need to monitor so access translates into safe, real-world outcomes. Repotrectinib listed for ROS1-positive NSCLC, including activity after prior TKIs and in resistant mutations, plus monitoring for dizziness and pneumonitis Durvalumab listed for muscle-invasive bladder cancer using the Niagara perioperative regimen, balancing survival gains with immune-related toxicity Three new pembrolizumab listings across cervical cancer, adjuvant renal cell carcinoma and perioperative head and neck cancer, with discussion of endpoints and eligibility Haematology additions including a BCMA bispecific for relapsed myeloma, an oral kinase inhibitor for higher-risk myelofibrosis and mogamulizumab for cutaneous T-cell lymphoma PBS price cuts via generics and biosimilars, plus expanded supervised prescribing for some medicines by nurse practitionersFollow The PBS Update for regular discussions of PBS listings and oncology policy changes affecting Australian healthcare professionals.Visit the Show Notes for links to the updates discussed in this episode and to send us audio feedback or questions for future episodes.

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Navigating Today and Shaping Tomorrow in ISM: Personalized Strategies With Current and Emerging KIT Inhibitors

Play Episode Listen Later Mar 31, 2026 14:15

CME credits: 0.25 Valid until: 31-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/navigating-today-and-shaping-tomorrow-in-ism-personalized-strategies-with-current-and-emerging-kit-inhibitors/54388/ This online educational activity explores the evolving role of KIT-targeted tyrosine kinase inhibitors (TKIs) in indolent systemic mastocytosis (ISM). Expert faculty discuss pivotal clinical data supporting the approval of avapritinib, a potent TKI that targets KIT D816V, in patients with ISM. They also highlight emerging clinical evidence on next-generation KIT TKIs, such as elenestinib and bezuclastinib, that are designed for enhanced selectivity and minimal brain penetration. Finally, faculty discuss how these agents may be sequenced and integrated into a personalized, multidisciplinary treatment approach aimed at durable symptom control and improved quality of life for patients with ISM.=

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CH in children with SCD and Asciminib for CML in the ASC4FIRST trial

Blood Podcast

Play Episode Listen Later Mar 26, 2026 13:35

In this week's episode, Blood editor Dr. Laura Michaelis interviews Drs. Alexander Bick and Jorge Cortes on their latest papers published in Blood. Dr. Cortes, the current EIC of Blood Global Hematology discusses "Asciminib Demonstrates Superior Efficacy and Safety in Newly Diagnosed Chronic Myeloid Leukemia in the ASC4FIRST Trial" wherein the planned secondary analysis showed a further efficacy advantage and a consistently favorable safety profile for asciminib relative to investigator-selected TKIs, especially second-generation TKIs. Dr. Bick discusses "Increased prevalence of clonal hematopoiesis in children with sickle cell disease" where targeted sequencing for CH mutations in 2318 children with SCD and 2957 controls and found that children with SCD have a higher prevalence of CH, and majority of CH cases identified were very small “micro-CH” clones, more work is needed to define the clinical significance of these clones.

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S16 Ep31: ctDNA Testing At Progression May Help Detect Resistance and Guide Sequencing in GIST: With Drs Jonathan Trent, MD, PhD, and Neeta Somaiah, MD

Play Episode Listen Later Mar 20, 2026 26:26

In today's episode of OncLive On Air®, Jonathan Trent, MD, PhD, and Neeta Somaiah, MD, sat down to discuss the evolving role of circulating tumor DNA (ctDNA) testing in gastrointestinal stromal tumors (GIST), as well as the importance of identifying both initial drivers of disease and secondary resistance mechanisms when approaching frontline treatment selection and overall therapeutic sequencing.Trent is a professor of medicine, associate director of Clinical Research, and director of the Sarcoma Medical Research Program at the University of Miami Miller School of Medicine, in Florida. Somaiah is a professor and chair of the Department of Sarcoma Medical Oncology in the Division of Cancer Medicine at The University of Texas MD Anderson Cancer Center in Houston.Drs Trent and Somaiah began their discussion by highlighting the rarity of GIST, underscoring the importance of evaluation at specialized sarcoma centers and comprehensive molecular testing to identify driver alterations.Somaiah then reviewed the molecular landscape of GIST, noting that approximately 70% to 80% of tumors harbor activating mutations in the KIT gene, while additional cases involve rarer alterations such as BRAF or NTRK fusions. Of note, resistance to imatinib (Gleevec) frequently emerges through secondary mutations in KIT exons 13 or 17, which can influence sensitivity to subsequent TKIs.ctDNA testing may help detect these resistance mechanisms, particularly at progression or when tissue is limited, enabling clinicians to refine sequencing strategies, both experts explained. They also discussed how mutation-informed approaches may guide treatment selection, including emerging strategies such as combining sunitinib (Sutent) with bezuclastinib to address resistant clones involving KIT exon 13 or 17 alterations.This content is a production of OncLive; this OncLive On Air podcast episode is supported by funding, however, content is produced and independently developed by OncLive.

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Navigating Therapeutic Advances in EGFR-Mutated NSCLC

ASCO Daily News

Play Episode Listen Later Mar 19, 2026 19:24

Dr. Monty Pal and Dr. Vamsi Velcheti discuss the evolving treatment landscape in EGFR-mutated non-small cell lung cancer, including landmark trials like FLAURA2, novel drug therapies, and the growing importance of ctDNA and MRD testing. TRANSCRIPT Dr. Monty Pal: Hello, and welcome to the ASCO Daily News Podcast. I'm your host, Dr. Monty Pal. I'm a medical oncologist and professor and vice chair of academic affairs at the City of Hope Comprehensive Cancer Center in Los Angeles. Today, I'm truly delighted to introduce Dr. Vamsi Velcheti, who's a professor of medicine and the chief of hematology-oncology at the Mayo Clinic in Jacksonville, Florida. We'll be discussing the expanding treatment landscape in EGFR-positive lung cancer and how to navigate the challenges of balancing treatment efficacy, toxicity, and patient quality of life in the EGFR-positive space. Just FYI, our full disclosures are available in the transcript of this episode. Vamsi, it's so great to have you on the podcast. Thank you so much for being here. Dr. Vamsi Velcheti: Thank you, Monty. It's a pleasure to be here with you. It's a really exciting topic and there are a lot of updates in the EGFR space. Dr. Monty Pal: So, I'm going to need your help with this because I'll be honest with you, I see very little lung cancer, if any, in my practice. I'm pretty much exclusively kidney cancer these days. I'm coming on 20 years at City of Hope now, and I still remember when trials like ECOG 1599 were presented with, you know, platinum doublets. And, of course, the field has changed a lot since then. But tell us a little bit about the first-line landscape, and I think just for the sake of time, we're going to stick with EGFR-positive disease here. What does it look like these days? Dr. Vamsi Velcheti: Monty, the foundation of care remains the third-generation EGFR inhibitors. These are selective EGFR inhibitors, like osimertinib. We've had an evolution of the development of these TKIs. Like, you know, we had the first-generation, second-generation, not-so-selective EGFR inhibitors. Now we have mutant-selective EGFR inhibitors in the clinic, and they're doing a really good job. And these are quite effective in patients who have classical activating mutations. But the reality is that these have not been transformative. These agents have fundamentally changed the response patterns, excellent CNS penetration, and very good tolerability profile. However, we don't see a lot of durability in terms of the response. So, what's different today is now there have been several trials in combination with these third-generation EGFR inhibitors that have really laid the foundation of how we kind of think about EGFR-positive disease. At the high level, there are a lot of challenges to selecting the patients for these combination-based modalities. I'm assuming we'll be talking more about these different trials and different approaches. Some of these combination-based strategies have really moved the needle in terms of improving overall survival and really improving long-term outcomes and durability in our patients. Dr. Monty Pal: And we are going to get into the weeds on this in just a moment. But I did kick off this podcast talking about chemotherapy, ECOG 1599. It does seem as though chemotherapy is still a component of management in advanced non-small cell lung cancer. So, can you tell us about, perhaps first, you mentioned osimertinib, you know, some of these next-generation EGFR inhibitors. Tell us about the role of chemo plus osimertinib. Dr. Vamsi Velcheti: That's exactly where I was going with the combination-based strategies. You know, we first started off with our earlier trials in the EGFR space evaluating the question of, are targeted therapies, are these highly effective, third-generation, EGFR-selective inhibitors, superior to platinum-doublet chemotherapy? And we've had multiple trials demonstrating that, like the FLAURA trial and in the past with second-generation EGFR inhibitors like erlotinib and gefitinib and afatinib. So, we know that these TKIs actually perform better than platinum-doublet chemotherapy. Now, we have a large, global, phase 3 trial data from the FLAURA2 trial, which looks at the question, "Hey, you know, osimertinib is better than chemotherapy, platinum-doublet chemotherapy. Can we do even better by combining osimertinib with platinum-doublet chemotherapy?" So, FLAURA2 answered that question. This is a large, phase 3 trial, and it's a positive trial with improved durability of disease control and improving overall survival with combination with chemotherapy. So, it's a very important and landmark trial, and essentially combining osimertinib with a platinum-based chemotherapy improved responses, deepened responses, and improved overall survival and really changing the disease trajectory. And this strategy is definitely compelling, especially in patients who have certain clinical high-risk features like, you know, patients who have high disease burden or patients who are sometimes having rapid disease progression early on osimertinib, especially with patients who have a lot of visceral disease burden. So, intensifying treatments up front could alter the natural trajectory of the disease. Dr. Monty Pal: So, you sort of alluded to this in that last part there, but is that kind of how you in clinical practice select? Is it based on, you know, visceral involvement? Is it based on rapidity of disease where you think about adding chemotherapy to osimertinib? Maybe you can give us the corollary. Which patients do you just use osimertinib alone in, for instance? Dr. Vamsi Velcheti: Definitely, there are some patients who have low disease burden and they have the classical mutations, like an exon 19 deletion. And these patients, especially if they don't have a lot of disease burden, they don't have CNS involvement, there may be a subset of patients who could just do fine on osimertinib of course, with close monitoring of the disease. I guess we'll get into that later, how do we do that with either ctDNA or like closer imaging or both. So, there may be some opportunity to kind of escalate patients' treatments based on certain clinical characteristics or radiographic characteristics or certain biological characteristics informed by ctDNA or other approaches. Dr. Monty Pal: No, that's interesting. And you're right, we will chat about ctDNA in just a bit. But before we get there, I think one of the big agents that has really sort of come to the fore in advanced non-small cell lung cancer is amivantamab. I've heard a lot about this in the context of even kidney cancer because in certain subsets, I'm interested in MET-directed therapies and so forth, right? So maybe tell us a little bit about the mechanism of amivantamab first, and then maybe tell us about this pivotal MARIPOSA trial where it's combined with lazertinib. Dr. Vamsi Velcheti: So, the MARIPOSA trial compared lazertinib alone with amivantamab plus lazertinib. And this trial demonstrated overall survival advantage, and there were key differences in terms of tolerability and the safety of amivantamab, which is an EGFR and MET bispecific, and there were certain kind of unique toxicity profiles that make it a little different than the intensification approach with chemotherapy through the FLAURA2 trial. So, there's a trade-off in terms of the toxicity profile. It's a different agent and a different management protocol in terms of dermatological toxicity management that clinicians need to be comfortable with. And also, there are certain unique issues in terms of amivantamab; there's a higher rate of infusion-related reactions, there's an increased risk for edema and VTEs because of amivantamab. Certainly a different toxicity profile, different management paradigm there in terms of longitudinal care of these patients requiring dermatological care and like, you know, close monitoring and prophylaxis VTEs. But having said that, definitely it's a different strategy, and it kind of changes the biology and the natural history of the cancers, and we do see some durability of responses that we see with the MARIPOSA. So, it's certainly a great alternative, at least for some patients. Dr. Monty Pal: That was a great overview of MARIPOSA. Now comes the really difficult question, which is, how do you choose between the two? You have these two great options, right, for EGFR-positive patients. You've already highlighted some of the distinctions in terms of toxicity. I think the audience is well aware of the side effects of chemo-doublet, perhaps even the EGFR-based therapies. Amivantamab is quite new. Give us a sense of how you in clinical practice decide between the two potential options here. Dr. Vamsi Velcheti: Yeah, I think that's the big challenge. I think these are two independent strategies that have evolved through the phase 3, and both of them have demonstrated overall survival benefit. So, the way I think about this is in three dimensions, right? Like, the disease biology, the patient priorities, and feasibility of care delivery. So, when I talk about the disease biology, you know, the mechanism is very different, and MET is a very dominant driver of disease in EGFR-altered patients and it's a significant mechanism of resistance, acquired resistance to TKIs. So, certainly I think there's a patient population that could benefit from a MET-directed therapy up front. However, we don't have great data to kind of really demonstrate how using amivantamab in the front line is going to change that. And are there like perhaps like some patients who we could identify who would benefit from such a strategy? Very recently, there have been some approvals in the second-line setting in lung cancer, not in the EGFR space, but like in generally in lung cancer, with the MET ADCs, and those drugs are approved with a companion diagnostic, which requires MET IHC testing. So, what has happened, at least in large academic practices and also I think in the community now, they have been checking for MET IHC expression more routinely in lung cancer. What we have been doing in our institution is we have been doing MET IHC as a reflex for all patients with EGFR, not just EGFR, but all non-small cell lung cancer patients. What that has done is now, like, we have been increasingly testing patients with EGFR for MET. And there's clearly a subset of patients who have de novo MET expression and a high MET expression. And those patients, I've been kind of like preferentially treating them with the MARIPOSA regimen. But again, I have to caution the audience that we still don't have data that MET IHC is going to help us make those decisions, whether it's better than like a FLAURA2 regimen. But however, in the second-line setting in the CHRYSALIS trial, we know that MET is a very powerful predictor of response to amivantamab. We really need more data there, but that's what I have been doing in my practice. But also, there's a lot of patient preference here. Like, there are some patients who don't want chemotherapy, and they want a non-chemotherapy approach. So, certainly there are some patients who prefer to have amivantamab. And now with the amivantamab, the subcutaneous version, the infusion reactions and the logistics of actual administration of amivantamab are more favorable with the subcutaneous approval. So, those are some of the elements that we need to take into account. Dr. Monty Pal: Well, I want to hone in on that because this subcutaneous administration route has been a big debate that I've seen on social media. Tell us, how much easier does it actually make the amivantamab experience? Does it cut down on the rash? Is it just infusion reactions? What's been your clinical experience? Vamsi Velcheti, MD: So, the subcutaneous administration of amivantamab has definitely improved the infusion reaction issue. Very rarely patients have infusion reaction now with the subcutaneous injections. And also, the infusion time is much, much shorter. Like we don't need a lot of infusion time, which is sometimes a challenge in busy infusion clinics. We need to take that into account. As far as the impact of the subcutaneous formulation on dermatological toxicity, we haven't really seen significant difference in terms of the intensity or rates of dermatological toxicity with subcutaneous. The benefits are really with the infusion reaction, the ease of administration. And interestingly, in the PALOMA trial, it also seems to be, even though this was not the primary endpoint of the study, there seems to be some suggestion that the subcutaneous amivantamab seems to have improved OS compared to the IV amivantamab. We don't really understand why, but that's a finding from the trial that's very intriguing. Dr. Monty Pal: That is really fascinating. I'm kind of curious to see how that's going to pan out. I'm going to shift gears a little bit here. And, you know, as we sort of close, I wanted to talk a little bit about biomarkers. I mean, this is obviously not a lung cancer-specific issue. It's something we think about across the board. But what I will say is that there are certain commonalities, and in bladder cancer, we think a lot now about ctDNA. But you've been way ahead of the game in lung cancer. Tell us how you guys use ctDNA, maybe both from the standpoint of monitoring for mutational status, but if you can, maybe offer some insights into some of these new MRD tests that are available too. Dr. Vamsi Velcheti: Yeah, it's rapidly evolving. Certainly, I think in the lung cancer space, you know, this has really kicked off in the lung cancer space with incorporating ctDNA into the workflow. Of course, you know, like baseline evaluation, we still kind of heavily rely on tissue genomic sequencing. But as you know, with targeted therapy, a lot of these patients have disease that evolves over time, and changes in terms of mutational pattern driving acquired resistance is a major issue across different molecular subtypes. And especially so in EGFR, when there are certain actionable opportunities associated with that transformation. So, we need to kind of have like a longitudinal snapshot of how we monitor these patients. So, the ctDNA has come to be like a tool that has now come to the forefront of clinical workflow, and almost all my patients who are having disease progression have ctDNA for kind of evaluating for resistance and informing treatment decisions, especially in EGFR. But having said that, there are a lot of challenges in terms of using ctDNA as a tool for monitoring. There are a lot of different types of assays and different platforms, and being able to use this as a quantitative tool that would be used along with the CT scans that we routinely use in clinical practice has been a challenge. And I think I would love to hear your perspectives as well, Monty, about how you're thinking about that in bladder and other disease contexts. But having said that, I think there's a lot of opportunity to incorporate ctDNA and MRD assays into clinical decision-making. Right now, in terms of clinical trials and clinical development, there have been some very interesting trials that are currently ongoing, especially in the EGFR space. We know that patients who clear ctDNA, based on some retrospective data and also like some retrospective-prospective data from trials that have already read out, that patients who clear ctDNA early with target therapy tend to do much better. They have a longer durability of response. There may be a subset of patients who have, even though they're having radiographic response, they have persistent ctDNA after a certain time point of initiation of targeted therapy. Those patients may require escalation of therapy. We don't yet know. I can't recommend that as a standard right now because we don't have clinical evidence to support that. But however, some of the clinical trials, like the ELIOS trial that's being done right now, that's actually completed enrollment, we'll hopefully see the results very soon. So, there is an emerging thought that instead of intensifying treatment for all patients with EGFR, there may be a population that may be just fine with frontline osimertinib monotherapy and introducing the intensification strategy at the time of emergence of MRD or progression on ctDNA before radiographic progression. So, there are a lot of adaptive molecular response criteria that we are kind of exploring in clinical trials that could inform how the future is going to look like for EGFR and other perhaps targeted therapies as well. So, it's fascinating, and I think there's a lot of opportunity there. Dr. Monty Pal: You know, you asked for my perspective. I actually think that what you highlighted there is the most interesting opportunity for ctDNA: the ability to de-escalate therapy. In terms of drug development, we've done so much to bring new therapies to patients, and now it's a bit of an embarrassment of riches, but the downside is that I feel like we tend to overtreat a lot of patients in the clinic. So, I definitely view MRD, you know, some of these other ctDNA techniques with methylation and so forth that may not be sort of tumor-dependent or bespoke could be incredibly, incredibly helpful. You touched on sort of the future, right, in this last section here with biomarkers. But give us a sense now in terms of novel drug therapies in the EGFR space. What are you most excited about moving forward in 2026 and beyond? Dr. Vamsi Velcheti: Yeah, I think there's a lot going on in this space, and not just this space, but across lung cancer and others as well. Like looking at the next generation of targets for ADCs. And I think a lot of these have to do with…so far in the drug development space, as you know, the improvements in clinical outcomes has been very incremental. So, we really need to make that big leap. And I think the big leap is not going to come from, in my opinion, from the next ADC, but it's going to come from how we tailor treatments and how we monitor disease better and how do we kind of incorporate the next treatment earlier and not wait for the radiographic progression. So, there's a lot of opportunity there to integrate biomarkers and dynamic biomarkers into clinical trial design and incorporating the recent advances in terms of drug design. You know, we have a lot of assets in the EGFR space, the next-generation EGFR inhibitors that are kind of designed with resistance in mind and rational combination, knowing when to introduce those combinations is also equally important. So, there's a lot going on, really exciting times to be in drug development. The one thing that I really hope will come to the forefront in drug development, not just for lung cancer, but all disease groups, is to kind of really be thoughtful about how we incorporate these really cool molecular monitoring tools and creating a composite score with imaging to be able to like really design the next generation of clinical trials. Dr. Monty Pal: You're so spot-on with that. I definitely think that we're getting to this point where, you know, we could think about the next BiTE, the next CAR-T, the next ADC. But, you know, maybe it's time for us to start really honing in on appropriate applications of these drugs, honing in on the right dose and what have you, because I definitely see some issues there. Vamsi, this has just been terrific. I really want to thank you so much for sharing your fantastic insights with us today on the ASCO Daily News Podcast, and I really appreciate all your efforts to move the field of lung cancer forward. Dr. Vamsi Velcheti: Thanks, Monty. I really enjoyed the conversation. Dr. Monty Pal: Yeah, this was terrific. And thanks to our listeners as well. If you value the insights that you hear from the ASCO Daily News Podcast, please take a moment to rate, review, and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Follow today's speakers:    Dr. Monty Pal  @montypal  Dr. Vamsi Velcheti @VamsiVelcheti Follow ASCO on social media:         ASCO on X   ASCO on Bluesky        ASCO on Facebook         ASCO on LinkedIn         Disclosures:      Dr. Monty Pal:     Speakers' Bureau: MJH Life Sciences, IntrisiQ, Peerview    Research Funding (Inst.): Exelixis, Merck, Osel, Genentech, Crispr Therapeutics, Adicet Bio, ArsenalBio, Xencor, Miyarsian Pharmaceutical    Travel, Accommodations, Expenses: Crispr Therapeutics, Ipsen, Exelixis   Dr. Vamsi Velcheti:  Honoraria: Galvanize Therapeutics Consulting or Advisory Role: Bristol-Myers Squibb, Merck, AstraZeneca/MedImmune, GSK, Amgen, Taiho Oncology, Novocure, Regeneron, Takeda, Janssen Oncology, Picture Health Research Funding (Inst.): Genentech, Trovagene, Eisai, OncoPlex Diagnostics, Alkermes, NantOmics, Genoptix, Altor BioScience, Merck, Bristol-Myers Squibb, Atreca, Heat Biologics, Leap Therapeutics, RSIP Vision, GlaxoSmithKline

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Highlights From the 2026 ASCO GU Cancers Symposium

ASCO Daily News

Play Episode Listen Later Mar 5, 2026 20:09

Dr. Monty Pal and Dr. Andrea Apolo discuss practice-changing studies and other novel approaches in bladder, kidney, and prostate cancers that were presented at the 2026 ASCO Genitourinary Cancers Symposium. TRANSCRIPT Dr. Monty Pal: Hello and welcome to the ASCO Daily News Podcast. I'm your host, Dr. Monty Pal. I'm a medical oncologist, professor and vice chair of academic affairs at the City of Hope Comprehensive Cancer Center in Los Angeles. And today is super exciting, we're highlighting key abstracts that were presented at the 2026 ASCO GU Cancers Symposium, and I'm just delighted to be joined by the chair of this year's meeting, who is also a dear friend, Dr. Andrea Apolo. Dr. Apolo serves within the Center for Cancer Research at the NCI as head of the Bladder Cancer Section, and she is also acting deputy chief of the Genitourinary Malignancies Branch. Welcome, Andrea, it is so great to have you on the podcast. Dr. Andrea Apolo: Oh, thank you so much for having me. What a great ASCO that we had, it is really exciting, lots of really great data. So I look forward to chatting about it. Dr. Monty Pal: Excellent. And you know, our full disclosures are available in the transcript of this episode in case our listeners want to have a peek. The theme of this year's GU meeting was "Patient-Centered Care: From Discovery to Delivery." I love that theme. And really, this is one of the most competitive meetings out there, more than 850 abstracts being presented on high-impact science. Andrea, I just wanted to get right into it and dive into what I think we both felt were some of the most exciting abstracts of the meeting. And the first of those is one that I know is near and dear to your heart, being a bladder cancer expert yourself, and that is the KEYNOTE-B15 study presented by Matt Galsky. Can you give us a flavor for what that study entailed and some of the key results? Dr. Andrea Apolo: Yeah, I think this was kind of the missing study that we have been waiting for since we saw the EV-302 data in metastatic disease in the frontline setting. We wanted to know how well this combination would work in muscle-invasive bladder cancer patients. And we saw half of that puzzle, you can say half of the piece of the puzzle, when we saw the data at ESMO, the EV-303 data in patients that were cisplatin-ineligible. And then now we are getting the full story with patients that are platinum-eligible, cisplatin-eligible, with the EV-304 data. So that study randomized patients to receive chemotherapy, so different than the EV-303 where the patients were randomized just to receive the radical cystectomy. These patients were randomized to receive neoadjuvant EV plus pembro and then adjuvant EV plus pembro versus neoadjuvant gemcitabine and cisplatin with no adjuvant component to the control arm. So I think this is a really, really important study. Dr. Monty Pal: And share with us some of the results because this in my mind is definitely practice-changing. This is one of those studies that I think you walked into the office on Monday and you are like, "Okay, this is what I am doing now," right? Dr. Andrea Apolo: Yeah. So the study was positive. The primary endpoint was event-free survival, and it met the primary endpoint. The secondary endpoint of overall survival was also met. So really, really great results. Consistent with what we saw with EV-303, the median event-free survival was not reached for the EV plus pembro arm, and it was 48 months for the patients receiving gem-cis. And then looking at the 24-month estimated event-free survival, it was 79% for the EV plus pembro and 66% for the chemo, the gem-cis arm. And that was a hazard ratio of 0.5. So that is really exciting. That is the event-free survival. And then the overall survival, the medians were not reached for either arm, but when you look at the 24-month estimated overall survival, it was 87% for the EV plus pembro versus 81% for the gem-cis, and that was a hazard ratio of 0.65. So very positive study. And then another question that we had was the pathologic CR rate. Very consistent with what we saw with the EV-303, the pathologic response rate was about 56% for the patients that received EV plus pembro and about 32%, 33% for the patients that received gem-cis. So very consistent with the findings that we have been kind of seeing in phase 2 studies, and this is a pT0N0, so that is important. Dr. Monty Pal: So Andrea, you know, I think that the big question in folks' minds is at this point, we see the data from NIAGARA, cis-gem-durva, we have now seen this data. Put it into context for us. Is there a patient in this day and age who maybe shouldn't get IO altogether, who should maybe get the NIAGARA regimen as opposed to EV-pembro in this context? What are your thoughts there? Dr. Andrea Apolo: Now, that is a great question. I would say with this data, it is very enticing to give EV pembro to our patients in the perioperative setting, and for that to be the new standard of care for all patients, regardless of cisplatin eligibility. So similar to what we saw with EV-302 really changing the standard of care in the frontline setting, I think these two studies, the EV-303 and the EV-304, change the standard of care for patients with muscle-invasive bladder cancer in the perioperative setting, and this should be the new standard of care if the patients don't have a restriction to receiving an immunotherapy. Dr. Monty Pal: I totally agree with that assessment. It is great to hear it from the expert's mouth as well. Thanks a lot for that, Andrea. The next abstract I wanted to tackle is one that is, I would say, near and dear to my heart because I know these folks really well. It is led by the SWOG group, and this is SWOG S1602. The number there for the audience gives you a sense of how long the study has been running for. The 16 prefix means it is something that we kicked off back in 2016. So this study is really 10 years in the making, right? So Rob Svatek presented this data. It is interesting, right, because it addresses this issue of the BCG (Bacille Calmette-Guérin) shortage, right, where we have needed to sort of rely potentially on other alternative sources or regimens and so forth. Tell us about this trial, Andrea. Dr. Andrea Apolo: This is one of my favorite studies. We talked about putting it in the main oral abstracts, but we put it in one of the educational sessions that talked about non-muscle-invasive bladder cancer because we thought that would be the best audience for it. But it doesn't take away from how important this abstract is, and the tremendous effort that went into the study. Almost a thousand patients enrolled. I think 984 were eligible to enroll in this study. So it is a very high enrolling, randomized, cooperative group study in high-grade non-muscle-invasive bladder cancer. And really the study was designed to address two questions. One is the BCG shortage and can we use a different strain, Tokyo versus TICE? And whether there is a priming effect if you gave intradermal BCG to patients with non-muscle-invasive bladder cancer, can that enhance the effect if you gave it a little bit earlier? I think the study is really important, and it met its primary endpoint, which was it is not inferior to TICE. The findings were really terrific in terms of the outcomes. Numerically. When you look at the endpoint, it looked like the Tokyo strain was as good, if not maybe a little bit better, but not statistically significant than the TICE. And then they broke it down by carcinoma in situ, they broke it down by papillary tumors, and the Tokyo strain was non-inferior in both of those instances. But interestingly, the intradermal BCG did not change outcomes. There was really no priming effect, which was really backed up by pre-clinical data that there would be, but there wasn't a priming effect when the intradermal BCG was given in the Tokyo strain. So that was a really, really interesting finding. But a great study, really important outcomes in the field for non-muscle-invasive bladder cancer. Dr. Monty Pal: Totally. And it just seems like we can't get away from BCG, right? You know, as hard as we try, I mean, I appreciate the studies that sort of build on it that are emerging right now, but it seems like BCG at least for the foreseeable future is kind of here to stay, right? Dr. Andrea Apolo: It works. It is one of the most effective treatments we have for non-muscle-invasive bladder cancer. So, you know, I think it is here to stay and, you know, we need to find alternatives in terms of strains so we don't deal with this shortage that we have been dealing with for so many years now. Dr. Monty Pal: Yeah, indeed. Moving on to some of the other highlighted studies from the meeting, you had mentioned the EV-303 data, so we probably don't need to rehash that study design in much detail. But there was also a rapid oral abstract presented by Dr. Ullén that I think is of interest here, right, that really hones in on pathologic outcomes and DFS from that trial. Do you mind just outlining that for our listenership? Dr. Andrea Apolo: This is the KEYNOTE-905, also known as the EV-303 study. This is a follow-up to the EV-303 data looking at the pathologic response rates, looking at the downstaging effect, looking at the surgical margins after treatment with the neoadjuvant EV plus pembro in the 303. Now, remember in the 303, patients got three cycles of neoadjuvant EV plus pembro and then six cycles in the adjuvant setting. A little bit different than the 304, where they got four cycles, which is really kind of the standard in the neoadjuvant setting, and then five cycles in the adjuvant setting. So still a total of nine cycles. But in the 303, the treatment arm had no systemic therapy, so it was just radical cystectomy. And they looked at the negative margins that you get with the EV plus pembro treatment, which was 92.6% versus 79% with patients receiving just the surgery alone. And then the pathologic CR rate, there was more follow-up on that, it was 57% for the patients receiving EV plus pembro, and as we would expect, about 9% for the patients that just went on to surgery alone because you can achieve a pathologic response rate with TURBT alone. Then they looked at the pathologic downstaging, so anything less than a pT2, and that was 66% in the patients that received the EV plus pembro. So very interesting findings, and it is also really just nice to have now the EV-304 data, like I was saying, there were two pieces of it, the cisplatin-eligible and the cisplatin-ineligible, and just to have those contemporary controls are really important. How did the cisplatin-ineligible do versus the cisplatin-eligible patient in terms of the event-free survival and in terms of the overall survival? So I feel like now we have all of this data that we can kind of put together in the perioperative setting and we can really inform our patients a little bit more about their outcomes depending on whether they are cisplatin-eligible or not, which you know cisplatin-ineligible patients often just, they are sicker, they may have obstruction, their tumors may be larger, they just tend to be a more delicate population than the cisplatin-eligible patients. So not surprisingly, you know, we see that in the EV-303 the disease-free survival for the patients is pretty poor. So the disease-free survival that was reported for this follow-up of the specific abstract was 23.6 months for the patients that just got surgery, and it was not reached for the patients that had the EV plus pembro, and that was a hazard ratio of 0.37. Dr. Monty Pal: Excellent, excellent distillation. So Andrea, in the interest of time, I mean, we could probably talk about bladder cancer forever, but I am going to move us on to the subject of kidney cancer. We have two late-breaking abstracts, LITESPARK-011, which looked at lenvatinib and belzutifan versus cabozantinib in the advanced setting, and then we have an adjuvant study, LITESPARK-022, that looked at pembrolizumab with or without belzutifan in the adjuvant setting. Both studies positive. One for progression-free survival, the other for disease-free survival. Both I think making a big dent in how we treat kidney cancer. Can you tell us a little bit about that? Dr. Andrea Apolo: Yeah, we have been waiting for these trials for a long time. So one of the things that we have been talking about at GU ASCO is to have plenary sessions. And if we would have had a plenary session, these two abstracts would have been part of it because they are important data, really big studies where we are trying to improve the outcomes of our patients with kidney cancer. So the first one, the LITESPARK-011, like you said, this is for advanced renal cell carcinoma, clear cell renal cell carcinoma, where we really don't have a standard of care after IO therapy, right? So we give IO-IO, we give VEGF-IO, but we don't really have a good standard of care. We usually give monotherapy TKIs. So the combination of belzutifan and lenvatinib versus what a standard of care is, cabozantinib, is really an important question to ask. And you know, this is a pretty large study, about 750 patients were randomized. And belzutifan plus lenvatinib demonstrated an improvement in progression-free survival and overall survival versus cabozantinib, but not overall survival, at least not yet, is what the authors are saying. So for the progression-free survival, the hazard ratio was 0.7 and it was 14.8 months for the combination, belzutifan plus lenvatinib arm versus cabozantinib, which was 10.7 months. So I think that is significant. And for the overall survival, it did favor the combination again with a hazard ratio of 0.85. The median was 35 months versus 28 months for the monotherapy cabozantinib, but it did not reach statistical significance. And the authors said that this will be further tested at a final analysis, these were the interim results. And for the overall survival, the overall survival was 53% for the combination versus 40%. This is significant. And the CR rates were lowish for both of them, it was like 5% for the combo and 1% for cabo monotherapy. So I think that the findings are important because we don't have a standard of care. And although there is no survival benefit, there was a trend. So I think this could be considered in patients that are fit, a treatment option for these patients in the later line settings. Dr. Monty Pal: Great points. I mean lots of great discussion around toxicity as well as efficacy. I mean certainly this is a regimen that may not be suitable for every patient in my portfolio, but certainly one to consider. Now Andrea, let's shift focus to LITESPARK-022, the adjuvant trial that I mentioned previously. So this is again looking at pembrolizumab with or without belzutifan, met the primary endpoint of disease-free survival. What are your impressions there of the data? Dr. Andrea Apolo: Yeah, the data looks great. And this was a really large study, 1,800 patients were randomized, and the study met the primary endpoint of disease-free survival, benefiting the combination of pembro plus belzutifan. And that is really terrific. The medians were not reached for either arm. And in terms of the overall survival results, also the medians were not reached, but the hazard ratio was 0.78 and did not reach a statistical significance. So there was again a statistically significant improvement in disease-free survival for the combination of pembrolizumab plus belzutifan, but not an overall survival benefit. So I guess, Monty, you know, we can kind of talk about what that means. There was a lot of discussion about belzutifan and some of the side effects, specifically anemia and managing anemia in this setting and requirements for transfusions. Generally, the authors said it was well tolerated, but we know that combination studies do have more toxicity. So it may be a select group of patients again, similar to the advanced setting, where we opt for a combination, possibly until we see more follow-up data in terms of the overall survival. Dr. Monty Pal: I have to agree with you. You know, in my group, we have been talking about a lot of pembrolizumab-based studies that are running right now, some through the NCI, some, you know, our own sort of homegrown investigator-sponsored trials, and you know, I think for the foreseeable future we are comfortable just maintaining pembrolizumab. Things might change if, for instance, we ultimately see a survival advantage emerge, but I just have my own personal doubts around that, that will be interesting. Okay, so now we are going to move to the last disease category that we are going to cover, which is prostate cancer. So there, we have the long-awaited results from the PEACE-3 study. These are the final OS results from this trial looking at enzalutamide with or without radium-223 in metastatic castration-resistant prostate cancer. So Andrea, would love to get your perspectives on this. Dr. Andrea Apolo: Yeah, so this study had been presented before and we had seen positive results for the combination of enzalutamide and radium with some interim overall survival results also showing a benefit. But like you said, these are the final results with a median follow-up of 58 months. So it was really nice to see the final results. And with the combination of enzalutamide and six cycles of radium, it did show an improvement in overall survival with a hazard ratio of 0.76. The median overall survival increased from 32.6 months to 38.2 months with the combination. So that is really great. There was some crossing over of the overall survival curves around 18 months was still seen. And again, there was also an improvement in the rPFS with a hazard ratio of 0.71, and the median rPFS improved from 16.4 to 19 months with the combination. So, you know, we have been awaiting the final results, but we kind of knew a lot about the benefits of the combination. And it is something that is kind of slowly trickling into the community in terms of adapting it and using it. There is more buzz now about it and I think these overall survival results will hopefully shift the community into incorporating the combination in these patients. Dr. Monty Pal: Brilliant. So well said. I mean, Andrea, congratulations on a terrific meeting. You have really done it again. Incredible, incredible output from this year's ASCO GU. I just want to thank you for joining us on the program today. Dr. Andrea Apolo: Oh, thank you so much for having me, Monty. It was really a joy to work with the ASCO team and with all the investigators and the Education Committee and the Scientific Committee. Everyone was really outstanding. So to me it was an honor to be part of this meeting, and I am so happy that it was so successful and really presented some amazing data that I think will be practice-changing to our patients. Dr. Monty Pal: Oh, thanks a ton. And also a huge thanks to our listeners. If you enjoyed the content of today's podcast, please don't forget to like and subscribe to our channel wherever you listen to podcasts. Thanks so much. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Follow today's speakers:    Dr. Monty Pal  @montypal  Dr. Andrea Apolo @apolo_andrea Follow ASCO on social media:         ASCO on X   ASCO on Bluesky        ASCO on Facebook         ASCO on LinkedIn         Disclosures:      Dr. Monty Pal:     Speakers' Bureau: MJH Life Sciences, IntrisiQ, Peerview    Research Funding (Inst.): Exelixis, Merck, Osel, Genentech, Crispr Therapeutics, Adicet Bio, ArsenalBio, Xencor, Miyarsian Pharmaceutical    Travel, Accommodations, Expenses: Crispr Therapeutics, Ipsen, Exelixis    Dr. Andrea Apolo: No disclosures to report.

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So You Think You Want a TKI?

Play Episode Listen Later Mar 4, 2026 6:00

CME credits: 0.75 Valid until: 04-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/So-You-Think-You-Want-a-TKI/54102/ This activity examines the evolving role of tyrosine kinase inhibitors (TKIs) in treating exudative retinal diseases such as wet age-related macular degeneration (AMD) and diabetic macular edema (DME). Experts discuss limitations of current anti-VEGF therapies, emphasizing challenges with durability and adherence. The series further explores TKI mechanisms and their formulation into sustained-release delivery systems. Detailed overviews of clinical programs (eg, LUGANO, LUCIA, SOL-1, SOL-R) highlight ongoing phase 3 studies evaluating efficacy and treatment intervals. Real-world case discussions further illustrate patient types who may benefit from these investigational agents. The conversation concludes with considerations for integrating TKIs into future practice. *Please stay tuned for additional content to this activity available for credit. The maximum amount of credit(s) available for the entire activity is 0.75.

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The Struggle Is Real

Play Episode Listen Later Mar 4, 2026 5:30

CME credits: 0.75 Valid until: 04-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/The-Struggle-Is-Real/54098/ This activity examines the evolving role of tyrosine kinase inhibitors (TKIs) in treating exudative retinal diseases such as wet age-related macular degeneration (AMD) and diabetic macular edema (DME). Experts discuss limitations of current anti-VEGF therapies, emphasizing challenges with durability and adherence. The series further explores TKI mechanisms and their formulation into sustained-release delivery systems. Detailed overviews of clinical programs (eg, LUGANO, LUCIA, SOL-1, SOL-R) highlight ongoing phase 3 studies evaluating efficacy and treatment intervals. Real-world case discussions further illustrate patient types who may benefit from these investigational agents. The conversation concludes with considerations for integrating TKIs into future practice. *Please stay tuned for additional content to this activity available for credit. The maximum amount of credit(s) available for the entire activity is 0.75.

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To Implant or to Inject?

Play Episode Listen Later Mar 4, 2026 5:15

CME credits: 0.75 Valid until: 04-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/To-Implant-or-to-Inject/54100/ This activity examines the evolving role of tyrosine kinase inhibitors (TKIs) in treating exudative retinal diseases such as wet age-related macular degeneration (AMD) and diabetic macular edema (DME). Experts discuss limitations of current anti-VEGF therapies, emphasizing challenges with durability and adherence. The series further explores TKI mechanisms and their formulation into sustained-release delivery systems. Detailed overviews of clinical programs (eg, LUGANO, LUCIA, SOL-1, SOL-R) highlight ongoing phase 3 studies evaluating efficacy and treatment intervals. Real-world case discussions further illustrate patient types who may benefit from these investigational agents. The conversation concludes with considerations for integrating TKIs into future practice. *Please stay tuned for additional content to this activity available for credit. The maximum amount of credit(s) available for the entire activity is 0.75.

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Who Needs a TKI? Identifying the Right Candidates

Play Episode Listen Later Mar 4, 2026 5:45

CME credits: 0.75 Valid until: 04-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/Who-Needs-a-TKI-Identifying-the-Right-Candidates/54101/ This activity examines the evolving role of tyrosine kinase inhibitors (TKIs) in treating exudative retinal diseases such as wet age-related macular degeneration (AMD) and diabetic macular edema (DME). Experts discuss limitations of current anti-VEGF therapies, emphasizing challenges with durability and adherence. The series further explores TKI mechanisms and their formulation into sustained-release delivery systems. Detailed overviews of clinical programs (eg, LUGANO, LUCIA, SOL-1, SOL-R) highlight ongoing phase 3 studies evaluating efficacy and treatment intervals. Real-world case discussions further illustrate patient types who may benefit from these investigational agents. The conversation concludes with considerations for integrating TKIs into future practice. *Please stay tuned for additional content to this activity available for credit. The maximum amount of credit(s) available for the entire activity is 0.75.

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TKI: The New TKO for Retinal Diseases

Play Episode Listen Later Mar 4, 2026 5:30

CME credits: 0.75 Valid until: 04-03-2027 Claim your CME credit at https://reachmd.com/programs/cme/TKI-The-New-TKO-for-Retinal-Diseases/54099/ This activity examines the evolving role of tyrosine kinase inhibitors (TKIs) in treating exudative retinal diseases such as wet age-related macular degeneration (AMD) and diabetic macular edema (DME). Experts discuss limitations of current anti-VEGF therapies, emphasizing challenges with durability and adherence. The series further explores TKI mechanisms and their formulation into sustained-release delivery systems. Detailed overviews of clinical programs (eg, LUGANO, LUCIA, SOL-1, SOL-R) highlight ongoing phase 3 studies evaluating efficacy and treatment intervals. Real-world case discussions further illustrate patient types who may benefit from these investigational agents. The conversation concludes with considerations for integrating TKIs into future practice. *Please stay tuned for additional content to this activity available for credit. The maximum amount of credit(s) available for the entire activity is 0.75.

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Beyond Chemotherapy in ALL: Emerging Bispecific Antibodies, CAR T-cell Therapies, and Evolving Treatment Strategies

CCO Oncology Podcast

Play Episode Listen Later Feb 27, 2026 38:32

In this episode, Dr Ibrahim Aldoss and Dr Bijal Shah discuss how immunotherapy has transformed the treatment landscape of acute lymphoblastic leukemia (ALL), particularly in relapsed/refractory B-cell ALL, including: CD19-directed CAR T-cell therapies Next-generation CD19 bispecific antibodies The evolving role of allogeneic transplant Presenters: Ibrahim Aldoss, MD Associate Professor Division of Leukemia Department of Hematology/HCT City of Hope National Medical Center Duarte, California Bijal Shah, MD, MS Senior Member, Department of Malignant Hematology Moffitt Cancer Center Tampa, Florida Link to full program: https://bit.ly/4cRjiUi Get access to all of our new podcasts by subscribing to the Decera Clinical Education [Oncology] Podcast on Apple Podcasts, YouTube Music, or Spotify. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

S16 Ep10: Optimizing TKI Sequencing and Ponatinib Dosing Strategies in CML: With Quinto Gesiotto, MD

Play Episode Listen Later Feb 25, 2026 12:19

In today's episode, we welcomed Quinto Gesiotto, MD, a malignant hematologist at Tampa General Hospital in Florida.In the exclusive interview, Dr Gesiotto explored the evolving role of TKIs in the treatment of patients with chronic myeloid leukemia (CML), including dosing patterns for ponatinib (Iclusig) in those with CML and other TKI data to emerge in the CML space at the 2025 ASH Annual Meeting and Exposition. Dr Gesiotto also provided detail on emerging data on novel strategies and agents, along with genetic mutations beyond BCR-ABL1 T315I the could drive more personalized treatment sequencing and improved risk stratification in CML in the future.

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S16 Ep4: Comprehensive Ph+ ALL Paradigm Knowledge Informs Frontline Ponatinib Use: With Nicholas Short, MD

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Play Episode Listen Later Feb 13, 2026 16:15

In today's episode, we spoke with Nicholas Short, MD. Dr Short is an associate professor in the Department of Leukemia of the Division of Cancer Medicine at the University of Texas MD Anderson Cancer Center in Houston.In our exclusive interview, Dr Short discussed evolving factors at play for the treatment of patients with Philadelphia chromosome (Ph)–positive acute lymphoblastic leukemia (ALL). He also noted how the TKI ponatinib (Iclusig) stacks up against other TKIs for Ph-positive ALL, in addition to evolving approaches that incorporate treatments like blinatumomab (Blincyto).

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How I Treat Series on Acute Lymphoblastic Leukemia

Blood Podcast

Play Episode Listen Later Jan 29, 2026 26:27

In this week's episode, Blood Associate editor Dr. Hervé Dombret interviews authors Drs. Sarah K. Tasian and David T. Teachey on their contributions to the How I Treat Series on acute lymphoblastic leukemia. Dr. Tasian's paper, “How I treat Philadelphia chromosome-like acute lymphoblastic leukemia in children, adolescents, and young adults” discusses the different classes of Ph-like ALL and reviews the recent trials investigating TKIs and immunotherapy specifically for this high-risk patient population. Dr. Teachey's paper, “How I treat ETP-ALL in children”, discusses the best current and emerging therapies that may be used in patients with ETP ALL, including nelarabine and other new agents, immunotherapy, and allogeneic HSCT.See the full How I Treat series in volume 145 issue 1 of Blood.

How I Treat Series on the 25th anniversary of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia

Blood Podcast

Play Episode Listen Later Jan 22, 2026 34:54

In this week's episode, Blood Associate Editor, Dr. Jason Gotlib leads a discussion about the How I Treat Series commemorating the 25th anniversary of the introduction of tyrosine kinase inhibitors in CML, featuring Drs. Neil Shah, Simona Soverini, Elisabetta Abruzzese, and Yves Chalandon. The introduction of TKIs revolutionized patient outcomes in CML, turning a poor prognosis—3 to 5 years life expectancy—to a manageable chronic condition. In this conversation, we'll cover management techniques for CML during relapse, pregnancy, and explore indications for hematopoietic stem cell transplantation. See the full How I Treat series in Volume 147 issue 4 of Blood.

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185. ESMO Awards - Episode 5

Oncology for the Inquisitive Mind

Play Episode Listen Later Jan 21, 2026 31:34

We're back, baby! Michael and Josh predicted their ESMO journey would have eons to run, and they weren't wrong! For our first episode back in 2026, we revisit the important coverage of ESMO 2025, highlighting advances in upper gastrointestinal tract and hepatobiliary cancers. This episode covers FGFR inhibitors (Bemartizumab), updates on the MATTERHORN trial, the use of immunotherapy with trastuzumab and FLOT in HER2-positive localised oesophageal carcinoma, and investigates the use of TKIs and the novel drug nofazinlimab for those with unresectable or metastatic hepatocellular carcinoma.A jam-packed episode that aims to over-deliver on information, laughter, and hope.2026 is going to be a big one!Studies:FORTITUDE-101MATTERHORNPHERFLOT/IKF-053NCT04669496For more episodes, resources and blog posts, visit www.inquisitiveonc.comPlease find us on Twitter @InquisitiveOnc!If you want us to look at a specific trial or subject, email us at inquisitiveonc@gmail.comArt courtesy of Taryn SilverMusic courtesy of AlisiaBeats: https://pixabay.com/users/alisiabeats-39461785/Disclaimer: This podcast is for educational purposes only. If you are unwell, seek medical advice.Oncology for the Inquisitive Mind is recorded with the support of education grants from our foundation partners Pfizer, Gilead Pharmaceuticals and Merck Pharmaceuticals. MSD provided virtual participation with ESMO. Our partners have access to the episode at the same time you do and have no editorial control over the content. Hosted on Acast. See acast.com/privacy for more information.

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Expanding Treatment Options for Breast Cancer: ADCs and Oral SERDs

ASCO Daily News

Play Episode Listen Later Jan 8, 2026 27:14

Dr. Monty Pal and Dr. Hope Rugo discuss advances in antibody-drug conjugates for various breast cancer types as well as treatment strategies in the new era of oral SERDs for HR-positive breast cancer. TRANSCRIPT Dr. Monty Pal: Hello, and welcome to the ASCO Daily News Podcast. I'm your host, Dr. Monty Pal. I'm a medical oncologist and vice chair of academic affairs here at the City of Hope Comprehensive Cancer Center, Los Angeles. Today, I'm thrilled to be joined by Dr. Hope Rugo, an internationally renowned breast medical oncologist and my colleague here at City of Hope, where she leads the Women's Cancers Program and serves as division chief of breast medical oncology. Dr. Rugo is going to share with us exciting advances in antibody-drug conjugates (ADCs) that are expanding treatment options in various breast cancer types. She'll also address some of the complex questions arising in the new era of oral SERDs (selective estrogen receptor degraders) that are revolutionizing treatment in the hormone receptor-positive breast cancer space. Our full disclosures are available in the transcript of this episode. Dr. Rugo, welcome, and thanks so much for being on the podcast today. Dr. Hope Rugo: Thank you. Pleasure to be here. Dr. Monty Pal: So, I'm going to switch to first names if you don't mind. The first topic is actually a really exciting one, Hope, and this is antibody-drug conjugates. I don't know if I've ever shared this with you, but I actually started my training at UCLA, I was a med student and resident there, and it was in Dennis Slamon's lab. I worked very closely with Mark Pegram and a handful of others. This is right around the time I think a lot of HER2-directed therapies were really evolving initially in the clinics. Now we've got antibody-drug conjugates. Our audience is well-familiar with the mechanism there but tell us about how ADCs have really started to reshape therapy for HER2-positive breast cancer. Dr. Hope Rugo: Yeah, I mean, this is a really great place to start. I mean, we have had such major advances in breast cancer just this year, I think really changing the paradigm of treating patients. But HER2-positive disease, we've been used to having sequenced success of new agents. And I think the two biggest areas where we've made advances in HER2-positive disease, which were remarkably advanced this year in 2025, have been in antibody-drug conjugates with trastuzumab deruxtecan and with new oral tyrosine kinase inhibitors (TKIs) that have less of a target on EGFR and more on HER2, so they have an overall more tolerable toxicity profile and therefore a potentially better efficacy in the clinic. At least that's what we're seeing with these new strategies that we couldn't really pursue in the past because of toxicities of the oral TKIs. So, although our topic is ADCs, I'm going to include the TKI because it's so important in our thinking about treating HER2-positive disease. In the metastatic setting, we've seen these remarkable improvements in progression-free and overall survival in the second-line setting with T-DXd, or trastuzumab deruxtecan, compared to T-DM1. And then sequencing ADCs with giving T-DXd after T-DM1 was better than an oral tyrosine kinase or a trastuzumab combination with standard chemotherapy. That was DESTINY-Breast03 and DESTINY-Breast02. So, then we've had other trials since then, and T-DXd has moved into the early-stage setting, which I'll talk about in just a moment. But the next big trial for T-DXd in HER2-positive disease was moving it to the first-line setting to supplant what has become an established treatment for now quite a long time: the so-called CLEOPATRA regimen, which used the combined antibodies trastuzumab, pertuzumab with a taxane as first-line therapy. And then we've proceeded on with maintenance with ongoing HP for patients with responding or stable disease. And we'd seen long-term data showing, you know, at 8 years there was a group of patients whose cancers had never progressed and continued improved overall survival. So, T-DXd was studied in DESTINY-Breast09, either alone or in combination with pertuzumab compared to THP. The patient population had received a little bit more prior treatment, but interestingly, not a lot compared to CLEOPATRA. And they designed the trial to be T-DXd continued until progression with or without pertuzumab versus THP, which would go for six cycles and then stop around six cycles, and then stop and continue HP. Patients who had hormone receptor-positive disease could use hormone therapy, and this is one of the issues with this dataset because, surprisingly in this dataset and one other I'll mention, very few patients took hormone therapy. And even in the maintenance trial, the HER2CLIMB-05, less than 50% took hormone therapy as maintenance. This is kind of shocking to me and highlights an area of really important education, that outcome is improved when you add endocrine therapy for hormone receptor-positive HER2-positive metastatic disease in the maintenance phase, and it's a really important part of treatment. But suffice it to say, you know, you're kind of studying continued chemo versus stopping chemo in maintenance. And T-DXd, as we all expected, in combination with pertuzumab was superior to THP in terms of progression-free survival, really remarkably improved. And you could stop the chemo with toxicity, but most people continued it with T-DXd. Again, not a lot of people got hormone therapy, which is an issue, and you stop the chemo in the control arm. So, this has brought up a lot of interest in trying to use T-DXd as an induction and then go to maintenance, much as we do with the CLEOPATRA regimen with hormone therapy. But it brings up another issue. So first, T-DXd is superior; it's a great treatment. Not everybody needs to have it because we don't know whether it's better to give T-DXd first or second with progression - that we need a little bit longer follow-up. But just earlier this week, interestingly, the third week of December, the U.S. FDA approved T-DXd in the DESTINY-Breast09 approach with pertuzumab. So as I mentioned earlier, there was a T-DXd-alone arm; that arm has not yet reported. So very interesting, we don't know if you need pertuzumab or not. So what about the maintenance? That's the other area where we've made a huge advance here. So, we all want to stop chemo and we want to stop T-DXd. You don't want somebody being nauseated for two years while they're on treatment, and also there's a small number of patients with mostly de novo metastatic HER2-positive disease who are cured of their disease. We'd like to expand that, and I think these new drugs give us the opportunity to improve the number of patients who might be cured from metastatic disease. So the first maintenance study we saw was adding palbociclib, the CDK4/6 inhibitor, to endocrine therapy and HP, essentially. There, we had a remarkable improvement in progression-free survival difference of 15.2 months: 29 to 44 months, really huge. At San Antonio this year, we saw data with this oral tyrosine kinase inhibitor tucatinib, already showed it was great in a triplet, but as maintenance in combination with HP, it showed also a remarkable improvement in progression-free survival. But the numbers were all shifted down. So in PATINA, the control arm was in the 24-month range; here it was the tucatinib-HP arm that was in the 25 months and 16 months for control. So there was a differential benefit in ER-negative and ER-positive disease. So I think we're all thinking that our ideal approach moving forward would be to give T-DXd to most patients, we see how they do, and treat to best response. And then, stop the T-DXd, start HP, trastuzumab, pertuzumab for ER-negative, with tucatinib for ER-positive with palbociclib. We also have early data that suggests that both approaches may reduce the development of brain metastases, an issue in HER2-positive disease, and delay time to progression of brain metastases as seen in HER2CLIMB-05 in very early data - small numbers, but still quite intriguing that you might delay progression of brain metastases with tucatinib that clearly has efficacy in the brain. So, I think that this is a hugely exciting advance for our patients, and these approaches are quickly moving into the early stage setting. T-DXd compared to standard chemo, essentially followed by THP, so a sequenced approach resulted in more pathologic complete responses than a standard THP-AC-type neoadjuvant therapy. T-DXd alone for eight cycles wasn't better, and that's interesting. We still need the sequenced non-cross-resistant chemo. But I think even more importantly, the data from DESTINY-Breast05 looking at T-DXd versus T-DM1 in patients with residual disease after neoadjuvant HER2-targeted therapy showed a remarkable improvement in invasive disease-free survival with T-DXd versus T-DM1, and quite early. It was a high-risk population, higher risk than the T-DM1 trial with KATHERINE, but earlier readout with a remarkable improvement in outcome. We expect to be FDA approved sometime in the first half of 2026. So then we'll get patients who've already had T-DXd who get metastatic disease. But my hope is that with T-DXd, maybe with tucatinib in the right group of patients or even sequenced in very high-risk disease, that we could cure many more patients with early-stage HER2-positive breast cancer and cure a subset, a greater subset of patients with de novo metastatic disease. Dr. Monty Pal: That's brilliant. And you tackled so many questions that I was going to follow up with there: brain metastases, etc. That was sort of looming in my mind. I mean, general thoughts on an ADC versus a TKI in the context of brain mets? Dr. Hope Rugo: Yeah, it's an interesting question because T-DXd has shown quite good efficacy in this setting. And tucatinib, of course, had a trial where they took patients with new brain mets, so a larger population than we've seen yet for the T-DXd trials, and saw that not only did they delay progression of brain metastases and result in shrinkage of existing untreated brain mets, but that patients who develop a new brain met, they could stay on the same assigned treatment. They got stereotactic radiation, and then the patients who were on tucatinib with trastuzumab and capecitabine had a further delay in progression of brain mets compared to those on the placebo arm, even after treatment of a new one that developed on treatment. So, I think it's hard. I think most of us for a lot of brain mets might start with the tucatinib approach, but T-DXd is also a very important treatment. You know, you're kind of trading off a diarrhea, some liver enzyme elevations with tucatinib versus nausea, which you really have to work on managing because it can be long-delayed nausea, and this risk of ILD, interstitial lung disease, that's about 12%, with most but not all trials showing a mortality rate from interstitial lung disease of just under 1 percent. In the early-stage setting, it was really interesting to see that with T-DXd getting four cycles in the neoadjuvant setting, a lot less ILD noted than the patients who got up to 14 cycles, as I think they got a median of 10 cycles in the post-surgical setting, there was a little bit more ILD. But I think we're going to be better and better at finding this earlier and preventing mortality by just stopping drug and treating earlier with steroids. Dr. Monty Pal: And this ILD issue, it always seems to resurface. There are drugs that I use in my kidney cancer clinic, everolimus, common to perhaps the breast cancer clinic as well, pembrolizumab, where I think the pattern of pneumonitis is quite different, right? What is your strategy for recognizing pneumonitis early in this context? Dr. Hope Rugo: Well, it is, and you know, having done the very early studies in everolimus where we gave it in the neoadjuvant setting and we're like, "Hmm, the patient came in with a cough. What's going on?" You know, we didn't know. And you have mouth sores, you know, we were learning about the drug as we were giving it. What we don't do with everolimus and CDK4/6 inhibitors, for example, is grade 1 changes like radiation pneumonitis, we don't stop, we don't treat it. We only treat for symptoms. But because of the mortality associated with T-DXd, albeit small, we stop drug for grade 1 imaging-only asymptomatic pneumonitis, and some of us treat with a half dose of steroids just to try and hasten recovery. We've actually now published or presented a couple of datasets from trials, a pooled analysis and a real-world analysis, that have looked at patients who were retreated after grade 1 pneumonitis or ILD and tolerated drug very well and none of them died of interstitial lung disease, which was really great to see because you can retreat safely and some of these patients stayed on for almost a year benefiting from treatment. So, there's a differential toxicity profile with these drugs and there are risk factors which clearly have identified those at higher risk: prior ILD, for example. A French group said smoking; other people haven't found that, maybe because they smoked more in France, I don't know. And being of Japanese descent is quite interesting. The studies just captured that you were treated in Japan, but I think it's probably being of Japanese descent with many drugs that increases your risk of ILD. And, you know, older patients, people who have hypoxia, those are the patients. So, how do we do this? With everolimus, we don't have specific monitoring. But for T-DXd we do; we do every nine weeks to start with and then every 12 weeks CT scans because most of the events occur relatively early. Somebody who's older and at higher risk now get the first CT at six weeks. Dr. Monty Pal: This is super helpful. And I have to tell you, a lot of these drugs are permeating the bladder cancer space which, you know, is ultimately going to be a component of my practice, so thank you for all this. We could probably stay on this topic of HER2-positive disease forever. I'm super interested in that space still. But let me shift gears a little bit and talk about triple-negative breast cancer and this evolving space of HR-positive, HER2-low breast cancer. I mean, tell us about ADCs in that very sort of other broad area. Dr. Hope Rugo: So triple-negative disease is the absolute hardest subset of disease that we have to treat because if you don't have a great response in the early stage setting, the median survival is very short, you know, under two years for the majority of TNBCs, with the exception of the small percentage of low proliferative disease subsets. The co-question is what do we do for these patients and how do we improve outcome? And sacituzumab govitecan has been one strategy in the later line setting that was shown to improve progression-free and overall survival, the Trop-2 ADC. We had recently three trials presented with the two ADCs, sacituzumab govitecan and the other Trop-2 ADC that's approved for HR-positive disease, datopotamab deruxtecan. And they were studied in the first-line setting. Two trials with SG, sacituzumab govitecan, those trials, one was PD-L1 positive, ASCENT-04. That showed that SG with a checkpoint inhibitor was superior, so pembrolizumab was superior to the standard KEYNOTE-355 type of treatment with either a taxane or gemcitabine and carboplatin with pembrolizumab for patients who have a combined positive score for PD-L1, 10 or greater. So, these are patients who are eligible for a checkpoint inhibitor, and SG resulted in an improved progression-free survival. The interesting thing about that dataset is that few patients had received adjuvant or neoadjuvant checkpoint inhibitor, which is fascinating because we give it to everybody now. But access is an issue and timing of the study enrollment was an issue. The other thing which I think we've all really applauded Gilead for is that there was automatic crossover. So, you could get from the company, to try and overcome some of the enormous disparities worldwide in access to these life-saving drugs, you could get SG through the company for free once you had blinded independent central review confirmation of disease progression. Now, a lot of the people who got the SG got it through their insurance, they didn't bill the company, but 80 percent of patients in the control arm received SG in the second-line setting. So that impacts your ability to look at overall survival, but it's an incredibly important component of these trials. So then at ESMO, we saw the data from SG and Dato-DXd in the first-line metastatic setting for patients who either had PD-L1-negative disease or weren't eligible for an immunotherapy. For the Dato study, TROPION-Breast02, that was 10 percent of the patients who had PD-L1-positive disease but didn't get a checkpoint inhibitor, and for the ASCENT-03 trial population it was only 1 percent. Importantly, the trials allowed patients who relapsed within a year of receiving their treatment with curative intent, and the Dato study, TB-02, allowed patients who relapsed while on treatment or within the first six months, and that was 15 percent of the 20 percent of early relapsers. The ASCENT trial, ASCENT-03, had 20 percent who relapsed between 6 and 12 months. The drugs were better than standard of care chemotherapy, the ADCs in both trials, which is very nice. Different toxicity profiles, different dosing intervals, but better than standard of care chemotherapy in the disease that's hardest for us to treat. And importantly, when you looked at the subset of early relapsers, those patients also did better with the ADC versus chemotherapy, which is incredibly important. And we were really interested in that 15 percent of patients who had early relapse. I actually think that six months thing was totally contrived, invented, you know, categorization and doesn't make any sense, and we should drop it. But the early relapsers were 15 percent of TB-02 and Dato was superior to standard of care chemo. We like survival, but the ASCENT trial again allowed the crossover to an approved ADC that improved survival and 80 percent of patients crossed over. In the Dato trial, they did not allow crossover, they didn't provide Dato, which isn't approved for TNBC but is for HR-positive disease, and they didn't allow, of course, pay for SG. So very few patients actually crossed over in their post-treatment data and in that study, they were able to show a survival benefit. So actually, I think in the U.S. where we can use approved drugs already before there's a fixed FDA approval, that people are already switching to use SG or Dato in the first-line setting for metastatic TNBC that's both PD-L1 positive for SG and PD-L1 negative for both drugs. And I think understanding the toxicity profiles of the two drugs is really important as well as the dosing interval to try and figure out which drug to use. Dr. Monty Pal: Brilliant. Brilliant. Well, I'm going to shift gears a little bit. ADCs are a topic, again, just like HER2-positive disease we could stay on forever. Dr. Hope Rugo: Huge. Yes. Dr. Monty Pal: But we're going to shift gears to another massive topic, which is oral SERDs. In broad strokes, right, this utilization of CDK4/6 inhibitors in the context of HR-positive breast cancer is obviously, you know, a paradigm that's been well established at this point. Where do we sequence in oral SERDs? Where do they fit into this paradigm? Dr. Hope Rugo: Ha! This is a rapidly changing area; we keep changing what we're saying every other minute. And I think that there are three areas of great interest. So one is patients who develop ESR1 mutations that allow constitutive signaling through the estrogen receptor, even when there's not estrogen around, and that is a really important mutation that is subclonal; it develops under the pressure of treatment in about 40 percent of patients. And it doesn't happen when you first walk in the door. And what we've seen is that oral SERDs as single agents are better than standard single-agent endocrine therapy in that setting. The problem that we've had with that approach is that we're now really interested in giving targeted agents with our endocrine therapies, not just in the first-line setting where CDK4/6 inhibitors are our standard of care with survival benefit for ribociclib and, you know, survival benefit in subsets with other CDK4/6 inhibitors, and abemaciclib with a numeric improvement. So we give it first line. The question is, what do you do in the second-line setting? Because of the recent data, we now believe that oral SERDs should be really given with a targeted agent. And some datasets which were recently presented, which I think have helped us with that, have been EMBER-3 and then the most recently evERA BC, or evERA Breast Cancer, that looked at the oral SERD giredestrant with everolimus compared to standard of care endocrine therapy with everolimus, where 100 percent of patients received prior CDK4/6 inhibitor and showed a marked improvement in progression-free survival, including in the subsets of patients with a short response, 6-12 months of prior response to CDK4/6 inhibitor and in those who had a PIK3CA pathway mutation. The thing is that the benefit looks like it's much bigger in the ESR1 mutant population, although response was better, PFS wasn't better in the wild type. So, we're still trying to figure that out. We also saw EMBER-3 with imlunestrant and abemaciclib as a second line. Not everybody had had a prior CDK4/6 inhibitor; they compared it to imlunestrant alone, but still the data was quite striking and seemed to cross the need for ESR1 mutations. And then lastly, we saw data from the single arms of the ELEVATE trial looking at elacestrant with everolimus and abemaciclib and showed these really marked progression-free survival data, even though single-arm, that crossed the mutation status. At least for the everolimus combination, abemaciclib analysis is still to come in the mutated subgroups. But really remarkable PFS, much longer. Single-agent fulvestrant after CDK4/6 inhibitor AI has a PFS in like the three-month range and in some studies, maybe close to five months. These are all at 10-plus months and really looking very good. And so those questions are, is it ESR1 mutation alone? Is it all comers? We'd like all comers, right? We believe in the combination approach and we're learning more about combinations with drugs like capivasertib and other drugs as we move forward. Everybody now wants to combine their targeted agent with an oral SERD because they're clearly here to stay with quite remarkable data. The other issue, so the second issue in the metastatic setting is, does it make a difference if we change to an oral SERD before radiographic imaging evidence of progression? And that was the question asked in the SERENA-6 trial where patients had serial monitoring for the presence of ESR1 mutations in ctDNA. And those who had them without progression on imaging could be randomized to switch to camizestrant with the same CDK4/6 inhibitor or stay on their same AI CDK4/6 inhibitor. And they showed a difference in progression-free survival that markedly favored camizestrant. But interestingly, the people who were on the standard control arm had an ESR1 mutation, we think AIs don't work, they stayed on for nine more months. The patients who were on the camizestrant stayed on for more than 16 months. And they presented some additional subset data which showed the same thing: follow-up PFS data, PFS2, all beneficial in SERENA-6 at the San Antonio [Breast Cancer Symposium]. So, we're still a little bit unclear about that. They did quality of life, and pain was markedly improved. They had a marked delayed time to progression of pain in the camizestrant arm. So this is all a work in progress, trying to understand who should we switch without progression to an oral SERD based on this development of this mutation that correlates with resistance. And, you know, it's interesting because the median time to having a mutation was 18 months and the median time to switch was almost 24 months. And then there were like more than 3,000 patients who hadn't gotten a mutation, hadn't switched, and were still okay. So screening everybody is the big question, and when you would start and who you would change on and how this affects outcome. Patients didn't have access to camizestrant in the control arm, something we can't fix but we have experimental drugs. We're actually planning a trial, I hope in collaboration with the French group Unicancer, and looking at this exact question. You know, if you switch and you change the CDK4/6 inhibitor and then you also allow crossover, what will we see? Dr. Monty Pal: We're coming right to the tail end of our time here, and I could probably go on for another couple of hours with you here. But if you could just give us maybe one or two big highlights from San Antonio, any thoughts to leave our audience with here based on this recent meeting? Dr. Hope Rugo: Yeah, I mean, I talked about a lot of those new data already from San Antonio, and the one that I'd really like to mention which I think was, you know, there were a lot of great presentations including personalized screening presented from the WISDOM trial by my colleague Laura Esserman, fascinating and really a big advance. But lidERA was the big highlight, I think, outside of the HER2CLIMB-05 which I talked about earlier in HER2-positive disease. And this study looked at giredestrant, the oral SERD versus standard of care endocrine therapy as treatment for medium and high-risk early-stage breast cancer. And what they showed, which I think was really remarkable with just about a three-year median follow-up, was an improvement in invasive disease-free survival with a hazard ratio of 0.7. I mean, really quite remarkable and so early. It looked as though this was all driven by the high-risk group, which makes sense, not the medium risk, it's too early. And also that there was a bigger benefit in patients who were on tamoxifen compared to giredestrant versus AI, but for both groups, the confidence intervals didn't cross 1. There's even a trend towards overall survival, even though it's way too early. I think that, you know, really well-tolerated oral drug that could improve outcome in early-stage disease, this is the first advance we've seen in over two decades in the treatment of early-stage hormone receptor-positive disease with just endocrine therapy. I think we think that we don't want to give up CDK4/6 inhibitors because we saw a survival benefit with abemaciclib and a trend with giving ribociclib in the NATALEE trial. So we're thinking that maybe one approach would be to give CDK4/6 inhibitors and then switch to an oral SERD or to have enough data to be able to give oral SERDs with these CDK4/6 inhibitors for early-stage disease. And that's all in the works, you know, lots of studies going on. We're going to see a lot of data with both switching 8,000 patients with an imlunestrant switching trial, an elacestrant trial going on, and safety data with giredestrant with abemaciclib and soon to come ribociclib. So, this is going to change everything for the treatment of early-stage breast cancer, and I hope cure more patients of the most common subset of the most common cancer diagnosed in women worldwide. Dr. Monty Pal: Super exciting. It's just remarkable to hear how this has evolved since 25 years ago, which is really the last time I sort of dabbled in breast cancer. Thank you so much, Hope, for joining us today. These were fantastic insights. Appreciate you being on the ASCO Daily News Podcast and really want to thank you personally for your remarkable contribution to the field of breast cancer. Dr. Hope Rugo: Thank you very much, and thanks for talking with me today. Dr. Monty Pal: You got it. And thanks a lot to our listeners today as well. You'll find links to all the studies we discussed today in the transcript of this episode. Finally, if you value the insights that you hear today on the ASCO Daily News Podcast, please rate, review, and subscribe wherever you get your podcasts. Disclaimer: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. Guest statements on the podcast do not express the opinion of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Follow today's speakers:   Dr. Monty Pal @montypal Dr. Hope Rugo  @hoperugo Follow ASCO on social media:       ASCO on X ASCO on Bluesky      ASCO on Facebook       ASCO on LinkedIn       Disclosures:     Dr. Monty Pal:   Speakers' Bureau: MJH Life Sciences, IntrisiQ, Peerview  Research Funding (Inst.): Exelixis, Merck, Osel, Genentech, Crispr Therapeutics, Adicet Bio, ArsenalBio, Xencor, Miyarsian Pharmaceutical  Travel, Accommodations, Expenses: Crispr Therapeutics, Ipsen, Exelixis  Dr. Hope Rugo:   Honoraria: Mylan/Viatris, Chugai Pharma  Consulting/Advisory Role: Napo Pharmaceuticals, Sanofi, Bristol Myer  Research Funding (Inst.): OBI Pharma, Pfizer, Novartis, Lilly, Merck, Daiichi Sankyo, AstraZeneca, Gilead Sciences, Hoffman La-Roche AG/Genentech, In., Stemline Therapeutics, Ambryx

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Challenging Cases in Second Line & Beyond Renal Cell Carcinoma (RCC) - Dr. David Braun

Play Episode Listen Later Nov 30, 2025 22:36

In this episode of the Oncology Brothers podcast, we dive into the rapidly evolving landscape of renal cell carcinoma (RCC) treatment, focusing on second-line therapies. We were joined by Dr. David Braun, a GU Medical Oncologist from Yale University, to discuss two challenging real-life cases. We explored the current standard of care for metastatic RCC, including the use of immune-oncology (IO) therapies and tyrosine kinase inhibitors (TKIs). Dr. Braun shared insights on treatment options following disease progression, the importance of understanding disease biology, and the nuances of NCCN guidelines. Key topics included: • The role of TKI options like Axitinib, Cabozantinib, and Tivozanib in second-line treatment • The impact of disease progression on treatment decisions • Side effect management and the importance of palliative care • The potential use of HIF-2 alpha inhibitors like Belzutifan in specific scenarios Join us for an informative discussion that emphasized patient-centered care and the significance of shared decision-making in oncology. Follow us on social media: •⁠ ⁠X/Twitter: https://twitter.com/oncbrothers •⁠ ⁠Instagram: https://www.instagram.com/oncbrothers •⁠ Website: https://oncbrothers.com/ If you enjoy our conversations, please leave us a review and let us know what topics you'd like us to cover in future episodes! Stay tuned for more insights into the rapidly evolving field of cancer treatment. We are the Oncology Brothers! #RCC #KidneyCancer #TKI #Immunotherapy #OncologyBrothers #GUOncology

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Managing Toxicities of ROS1 Inhibitors in Non-Small Cell Lung Cancer (NSCLC) – Dr. Estela Rodriguez

Straight From The Cutter's Mouth: A Retina Podcast

Play Episode Listen Later Nov 13, 2025 16:11

Welcome to the Oncology Brothers podcast! In this episode, we dive into the management of ROS1 fusion positive non-small cell lung cancer (NSCLC) and explore the various tyrosine kinase inhibitors (TKIs) available for this rare subset of patients. Join us along with special guest Dr. Estelamari Rodriguez, a thoracic medical oncologist from Sylvester Comprehensive Cancer Center, as we discussed: • The importance of comprehensive next-generation sequencing (NGS) in management of NSCLC. • A detailed overview of ROS1 TKIs, including crizotinib, repotrectinib, entrectinib, taletrectinib. • Common side effects associated with these agents, such as fatigue, dizziness, edema, and liver toxicity. • Clinical pearls for managing adverse events and optimizing patient care. • The significance of patient education and regular follow-ups in ensuring treatment adherence and safety. Whether you're a healthcare professional or someone interested in oncology, this episode provides valuable insights into the practical aspects of treating ROS1 fusion positive NSCLC. Follow us on social media: •⁠ ⁠X/Twitter: https://twitter.com/oncbrothers •⁠ ⁠Instagram: https://www.instagram.com/oncbrothers •⁠ Website: https://oncbrothers.com/ Don't forget to check out our other ToxCheck episodes, conference highlights, and treatment algorithms. Subscribe for more discussions on bridging the gap between academic research and community practice! #ROS1 #NSCLC #TKIs #Crizotinib #Repotrectinib #Entrectinib #Taletrectinib #TargetedTherapy #OncologyBrothers #LungCancer

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Episode 484: November 2025 Retinal Physician preview including TKIs, Fluorinated Gas and Sustainability, Best Practices for Clinical Trial Sites, and Fellowship Selection Advice

Play Episode Listen Later Nov 10, 2025

Drs. Kat Talcott and Sarwar Zahid join to discuss the December 2025 edition of Retinal Physician, including an overview of TKIs for retinal disease, the fluorinated gas and sustainability question, best practices for research clinical trial sites, and fellowship selection advice.

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Managing Toxicities of Tyrosine Kinase Inhibitors (TKI) in CML - Drs. Onyee Chan & Fadi Haddad

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Play Episode Listen Later Nov 10, 2025 21:56

In this episode of the Oncology Brothers podcast, we are joined by esteemed hematologists Dr. Onyee Chan from Moffitt Cancer Center and Dr. Fadi Haddad from MD Anderson to discuss the management of side effects associated with tyrosine kinase inhibitors (TKIs) used in the treatment of chronic myeloid leukemia (CML). Join us as we delve into: • An overview of the different generations of TKIs, including imatinib, dasatinib, nilotinib, bosutinib, ponatinib, and asciminib. • Common class-wide toxicities such as fatigue, hypertension, gastrointestinal symptoms, and cytopenias. • Unique side effects associated with each TKI and strategies for dose optimization. • The importance of patient education and monitoring to ensure effective management of side effects. Don't forget to check out our other ToxCheck episodes on antibody drug conjugates, CAR-T therapies, and more! Follow us on social media: •⁠ ⁠X/Twitter: https://twitter.com/oncbrothers •⁠ ⁠Instagram: https://www.instagram.com/oncbrothers •⁠ Website: https://oncbrothers.com/ Subscribe to the Oncology Brothers for more discussions on bridging the gap between academic research and community practice in cancer care! #CML #TKI #ToxCheck #Hematology #OncologyBrothers #PrecisionMedicine

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First-Line Strategies in HER2+ Lung Cancer

PVRoundup Podcast

Play Episode Listen Later Oct 31, 2025 14:53

Drs. Cooper and Rotow discuss first-line treatment strategies for HER2+ NSCLC, highlighting the importance of comprehensive molecular testing and emerging targeted therapies. Key considerations include the efficacy of antibody-drug conjugates and TKIs, with ongoing clinical trials evaluating their potential as frontline treatments. The discussion emphasizes the need for personalized treatment approaches based on individual patient characteristics, molecular features, and the evolving landscape of HER2-targeted therapies.

Treating and Managing Chronic Myeloid Leukemia (CML) in 2025: Dr. Jorge Cortes