Podcast
ASCO Daily News
Hosted by American Society of Clinical Oncology (ASCO) · EN
The ASCO Daily News Podcast features oncologists discussing the latest research and therapies in their areas of expertise.
31episodes
Episodes
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Day 5: Top Takeaways From ASCO26
Yesterday00:09:35Tap to summarizeDr. Monty Pal shares highlights from the final day of ASCO26, including new research on treating anemia in myelofibrosis, advances in RAS-mutated mCRC, novel therapies for AML, and a potentially practice-changing trial in TNBC. LINK TO FULL TRANSCRIPT
Transcribe →Day 4: Top Takeaways From ASCO26
2d ago00:08:45Tap to summarizeDr. Monty Pal shares highlights from Day 4 of the 2026 ASCO Annual Meeting, including a much-anticipated study in hepatocellular carcinoma, new data in non–small cell lung cancer, and a key update in the treatment of Merkel cell carcinoma. LINK TO TRANSCRIPT
Transcribe →Day 3: Top Takeaways From ASCO26
3d ago00:08:54Tap to summarizeDr. Monty Pal shares highlights from Day 3 of the 2026 ASCO Annual Meeting, including new research for the treatment of advanced CRC and mCRPC, TIL cell therapy in advanced non-uveal melanoma, and an ultra-low dose immunotherapy trial in head and neck squamous cell carcinoma. LINK TO FULL TRANSCRIPT
Transcribe →Day 2: Top Takeaways From ASCO26
4d ago00:08:19Tap to summarizeDr. Monty Pal shares highlights from Day 2 of the 2026 ASCO Annual Meeting, including a practice-changing trial in renal cell carcinoma, advances in ER-positive, HER2-negative early breast cancer, and the use of olanzapine as an effective steroid-sparing alternative for chemo-induced nausea and vomiting in pediatric cancer. LINK TO FULL TRANSCRIPT
Transcribe →Day 1: Top Takeaways From ASCO26
5d ago00:07:54Tap to summarizeIn the first episode of a special daily series during the 2026 ASCO Annual Meeting, Dr. Monty Pal discusses 3 abstracts, including a follow-up on the EV-302 study in urothelial carcinoma, a potential new treatment option for patients with PD-L1-positive advanced non–small cell lung cancer, and a novel psychosocial digital application that improves fatigue and distress in patients with multiple myeloma. LINK TO FULL TRANSCRIPT
Transcribe →ASCO26 Preview: Novel Therapies and Innovations in Cancer Care
2w ago00:23:54Tap to summarizeDr. Monty Pal and Dr. Jo Chien preview new research, hot topics, and emerging innovations in oncology that will be presented at the 2026 ASCO Annual Meeting. LINK TO FULL TRANSCRIPT
Transcribe →The Future of AI in Oncology: A Conversation With Google's AI Innovators
3w ago00:27:23Tap to summarizeGoogle DeepMind's Dr. Alan Karthikesalingam and Google research scientist Anil Palepu sit down with Dr. Monty Pal to discuss the potential of Articulate Medical Intelligence Explorer (AMIE), a large language model-based experimental medical AI system designed to augment clinical decision-making in oncology and beyond, as well as the future of AI-human collaboration and how it could reshape health care over the next decade. LINK TO FULL TRANSCRIPT
Transcribe →'No Margin for Error': What to Know Before Implementing AI in Clinical Practice
Apr 1600:18:20Tap to summarizeDr. Monty Pal and Dr. Arturo Loaiza-Bonilla discuss the institutional risks in the use of artificial intelligence (AI) in clinical practice and how overreliance on AI could erode essential skills. They also highlight practical approaches, including routine "AI-off" drills, to help oncologists retain their decision-making agility. LINK TO FULL TRANSCRIPT
Transcribe →Groundbreaking Results Shift Treatment Paradigm in High-Risk Smoldering Multiple Myeloma
Apr 200:19:38Tap to summarizeDr. Monty Pal speaks with internationally acclaimed hematologists Dr. Vincent Rajkumar and Dr. Saad Usmani about the AQUILA trial in high-risk smoldering multiple myeloma, as well as advances in CAR-T and other evolving treatment strategies in the myeloma space. TRANSCRIPT Dr. Monty Pal: Hello everyone and welcome to the ASCO Daily News Podcast. I'm your host, Monty Pal. I'm a medical oncologist, underline medical oncologist, a professor, and vice chair of academic affairs at the City of Hope Comprehensive Cancer Center in Los Angeles. You're going to understand why I underlined "medical oncologist" there. I'm actually on the line today with two amazing hematologists. Today, we're going to actually explore treatments for high-risk smoldering multiple myeloma following the FDA's approval last year of daratumumab for the first-ever treatment of this indication. Now, this is based on the AQUILA trial, and this represents a huge shift in our traditional watch-and-wait approach to active disease interception. We're going to consider whether this landmark trial published in The New England Journal translates to day-to-day practice. I think it does, and we'll certainly make an argument for that. And I'm so fortunate today to have two internationally acclaimed experts here in the conversation: Dr. Vincent Rajkumar, senior author on the manuscript, and Dr. Saad Usmani, also an expert in his own right in myeloma. Dr. Rajkumar is the lead investigator of the AQUILA study. He's a professor of medicine and consultant in the divisions of hematology and hematopathology at the Mayo Clinic in Rochester, Minnesota. He actually chairs the Myeloma, Amyloidosis, Dysproteinemia Program. He is also editor-in-chief of the Blood Cancer Journal. Dr. Usmani, he and I actually go way, way back. We actually did the AACR Molecular Biology in Clinical Oncology course, I want to say in 2006, so this is our 20-year anniversary, Saad. He's the chief of the myeloma service at the MSK Cancer Center and a professor of medicine at the Weill Cornell Medical College in New York. Saad, Vincent, welcome. Dr. Saad Usmani: Thank you so much for having me, Monty. Dr. Vincent Rajkumar: Yeah, thanks, Monty. A pleasure to be here. Dr. Monty Pal: Thanks. And just a quick note for our listeners, all of our disclosures are available in the transcript of this episode. First off, Saad, did I get that right? Was it 2006 when we did that course together? Dr. Saad Usmani: Yeah, 20 years. We are coming up to our 20-year anniversary. It's remarkable to have seen our careers move the way they have, Monty. Dr. Monty Pal: Oh my gosh. And for all the fellows who are on the line, that AACR Molecular Biology and Clinical Oncology course, it's sometimes overlooked. Wonderful primer on translational science. Okay, now we're going to get to the heart of the matter here, the AQUILA trial. So this was a study, Vincent, that you led. I wonder if you'd walk us through the primary endpoints in the study. What are we looking at in the AQUILA trial specifically? Dr. Vincent Rajkumar: Thanks so much. Again, as you mentioned, smoldering multiple myeloma has just been a condition that we watch and wait. And the first thing that I want to clarify here is that the AQUILA trial is looking at only a subset of smoldering multiple myeloma. That is the high-risk smoldering multiple myeloma. It was defined the way high-risk smoldering myeloma was defined at the time the trial was designed. It randomized 390 patients. One arm got daratumumab single agent in an attempt to delay progression to active myeloma and possibly prolong survival. And the other arm was the traditional observation. The primary endpoint, therefore, was time to active multiple myeloma. Other endpoints included time to when patients needed to start therapy for active multiple myeloma, which can vary based on physician judgment, and overall survival. Of course, response rate, complete response rate, and others were also endpoints. Dr. Monty Pal: That's interesting. And you know, I wanted you to riff a little bit on this definition of high-risk smoldering myeloma. Can you tell our audience how that's sort of evolved over the years? Dr. Vincent Rajkumar: Yes. I mean, if you step back, monoclonal gammopathy of undetermined significance has only a 1% per year risk of progression. Smoldering multiple myeloma, all comers have a 10% per year risk of progression. And over the years, trials have been done in the whole population, and then more recently, we felt we should really focus on the people with high-risk smoldering, defined as a 50-50 risk of progression in 2 years. That's like a 25% per year risk of progression in the first 2 years, which is a very high risk for the patient and something that would justify prophylactic intervention. And that definition initially was based on just high levels of monoclonal protein like more than 3 grams, the IgA subtype of myeloma, the suppression of uninvolved immunoglobulins. Others have used bone marrow flow cytometry markers, cytogenetics. Those combinations of factors were available at the time the AQUILA trial was designed, and a select combination was used. Later on, we found that we could match almost all of that in a very simple risk stratification using just the percentage of bone marrow plasma cells, the level of the M-spike, and the free light chain ratio, all three of which are available to all patients with smoldering at the time of diagnosis. So you don't need any special testing. So more than 20% plasma cells, more than 20 for the light chain ratio, and more than 2 grams for the M-spike. If someone has any two of the three, that is high-risk smoldering multiple myeloma according to the IMWG, but that definition, of course, came in 2020 after the AQUILA trial completed accrual. Dr. Monty Pal: That's interesting because this sort of flips the traditional paradigm where biomarkers get more and more complex as time goes on. Am I right in saying this sort of simplifies things a little bit? It uses standard laboratory or clinical parameters to gauge this category? Dr. Vincent Rajkumar: Absolutely. People were using suppression of uninvolved immunoglobulins, and those levels are not standardized, often vary by race. Also, the other aspect was the abnormal plasma cells on flow cytometry. Again, labs define it differently. So this makes it much more simple. But the IMWG also did a separate exploratory cohort within that paper where we added cytogenetics and we added scoring systems to improve on this further. So it simplified it for regular clinical practice and for like trials. But if you have a patient in front of you, the IMWG paper also has more complex scoring systems where you can take more than 20; 21 is more than 20, so is 51. And so, you can use the actual numbers that a patient has, additional variables like cytogenetics, and get a more refined estimate of what is the true risk of progression. Dr. Monty Pal: That's really helpful. Now, you told us about the primary endpoints, you've helped us define high-risk smoldering myeloma. Can you give us a sense of the top-line results from AQUILA? Dr. Vincent Rajkumar: Yes, I think the most important one was the primary endpoint, time to multiple myeloma, was at 5 years, the progression-free survival was 63% in the daratumumab arm compared to 41% in the observation arm. So, you know, approximately 60% of patients in the observation arm had already progressed by 5 years. And that number was about 40% for the daratumumab arm. We also looked at time to starting myeloma therapy, which is clinically actually quite meaningful because, you know, myeloma therapy means patients get a quadruplet for induction, they get stem cell transplant, they get endless maintenance, they get ongoing therapy virtually for the entire duration. So, preventing the need for myeloma therapy is in and of itself, I think, a major endpoint. And that at 3 years, 40% of people in the observation arm required full myeloma therapy compared to only 20% in the daratumumab arm. So there's a significant reduction in the risk of developing active myeloma as well as the need for myeloma therapy by using a time-limited 3 years of daratumumab single agent. Dr. Monty Pal: Perfect summary of the results. And maybe, Saad, I'm going to bring you into the conversation now. How does this sort of influence your day-to-day practice for smoldering myeloma? Is this something that you've incorporated for that high-risk subset? Dr. Saad Usmani: Thank you, Monty, and I agree. I think that's a really nice summary from Vincent. This study is very important for several reasons. It's actually the third clinical trial that has demonstrated that patients who are in the high-risk smoldering myeloma category benefit from an early intervention that delays the progression to active myeloma or to end-organ damage. And so having a nuanced discussion with our patients in the clinic becomes very important. Having this discussion around as an option becomes very important. And like Vincent said, when we look at that high-risk smoldering myeloma patient population, someone who has 22, 23% plasma cells versus, you know, 45, 50, you know, it's going to be a different discussion each time. But I think it's a very important first step. And I think this sets up the stage for ...
Transcribe →Navigating Therapeutic Advances in EGFR-Mutated NSCLC
Mar 1900:19:24Tap to summarizeDr. 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...
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