Podcasts about dana farber cancer institute

Dr Sarah Sammons from Dana-Farber Cancer Institute in Boston, Massachusetts, discusses cases and reviews the current management of brain metastases in patients with HER2-positive breast cancer. CME information and select publications here.

Hart and Fitzy recap a record-setting WEEI/Nesn Jimmy Fund Radio-Telethon where we raised $5.7 million for The Jimmy Fund and Dana-Farber. The Red Sox dropped a two game series to the Orioles in rough fashion after failing to convert with runners in scoring position multiple times.

Hart and Fitzy recap a record-setting WEEI/NESN Jimmy Fund Radio-Telethon. Why didn't the Red Sox send Nate Eaton home last night in extra innings? Could their upcoming series with the Yankees determine the season?

Emily Bailey, nurse navigator, Jimmy Fund Clinic, Dana-Farber Cancer Institute, and Amelia “Mia” McDonough, nurse, Jimmy Fund Clinic, Dana-Farber Cancer Institute ● Emily graduated from University of North Carolina Wilmington in 2018. She has been a nurse for eight years transitioning from the population of adult solid tumor oncology to pediatric oncology. ● At the Jimmy Fund Clinic, she is solid tumor nurse navigator. As a nurse navigator, she assists with guiding young patients and their families through the complex cancer diagnosis and treatment. They coordinate care and provide continuous education and support. ● In her free time, Emily enjoys running and will be running the Boston Half presented by Dana-Farber and Jimmy Fund in November. About Mia McDonough ● Amelia grew up in Dedham and graduated from Villanova University in Pennsylvania. She's had multiple family members treated at Dana-Farber as adult patients and always knew Dana-Farber was a special place. ● Amelia joined the Jimmy Fund Clinic as a nurse in 2024. In the infusion room, she has anywhere from four to six patients per day - they maybe getting chemotherapy, blood products, or coming in for sick visits. She is responsible for coordinating with their providers to make sure they get all they need while they're in the infusion chair.

Christopher Lathan, MD, Chief Clinical Access Officer, Dana-Farber Cancer Institute ● Dr. Christopher Lathan is the Chief Clinical Access Officer at Dana-Farber, founding Director of the Cancer Care Access Program and a clinical oncologist focusing on lung cancer. ● His research is centered on the effects of race, class, and access to care in cancer outcomes, including racial disparities in lung cancer treatment, differences in access to precision medicine by race and social class and equitable distribution of new treatment across historically marginalized populations. ● Dr. Lathan aims to bridge the gap between research in disparities and the realities of patient care by developing interventions to increase access to high quality care, developed in part through community engagement.

Christopher Lathan, MD, Chief Clinical Access Officer, Dana-Farber Cancer Institute ● Dr. Christopher Lathan is the Chief Clinical Access Officer at Dana-Farber, founding Director of the Cancer Care Access Program and a clinical oncologist focusing on lung cancer. ● His research is centered on the effects of race, class, and access to care in cancer outcomes, including racial disparities in lung cancer treatment, differences in access to precision medicine by race and social class and equitable distribution of new treatment across historically marginalized populations. ● Dr. Lathan aims to bridge the gap between research in disparities and the realities of patient care by developing interventions to increase access to high quality care, developed in part through community engagement.

Anne Gross, PhD, RN, FAAN, Senior Vice President of Patient Care Services, Chief Nursing Officer, Ning Zhao Chair of Nursing, Dana-Farber Cancer Institute ● Anne is responsible for adult and pediatric nursing across all care sites at Dana-Farber, The Phyllis F. Cantor Center for Research in Nursing and Patient Care Services, and the Center for Clinical and Professional Development. She also oversees a variety of other clinical services, patient and family programs, and Volunteer Services. ● Since joining Dana-Farber in 2002, she has led implementations of a primary nursing care model and a residency training program for newly licensed nurses and has secured funding for programs and research to support inclusion, diversity and equity, positive practice environments, and self-care and renewal programs. She also is involved in committees, boards, and initiatives nationally and internationally and is a Fellow in the American Academy of Nursing.

Dan Shaughnessy has watched The Jimmy Fund evolve throughout his time in Boston sports media. He also is confident that the Red Sox are a playoff team this season.

Charlie Davies breaks down his soccer comeback after being involved in a car accident, and how his recovery and support of his wife and children led to discovering he had Liposarcoma. He has been an avid supporter of Dana-Farber and The Jimmy Fund.

HR 4: Greg, Alma, Emilia, and Daniel Sarantopoulos, Daniel Sentana Lledo, and Will Flemming join the show on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon

Dr. Wolfram Goessling, Andrew Wagner, Olivia, Brittany, Joshua, and Owen Kazanjian, Hunter Henry, and Howes Products join the show on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon

Angel Kaifer, Joaquim Bellmunt, Kate Pingeon, and Marios Giannakis join the show on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon

Jason Marton, Matt Yurgelun, Dan Shaughnessy, Heather, Pasi Janne, and Charlie Davies join the show on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon.

Red Sox play-by-play broadcaster Will Flemming joins Jones and Keefe on day one of the WEEI/NESN Jimmy Fund Radio-Telethon. Will thinks the Red Sox low leverage relievers need to be better. He also thinks Garrett Crochet can win the Cy Young award this season, and prospects like Payton Tolle could help the Major League team this season.

HR 1: Jason Marton, Matt Yurgelun, Dan Shaughnessy, Heather, Pasi Janne, and Charlie Davies join the show HR 2: Angel Kaifer, Joaquim Bellmunt, Kate Pingeon, and Marios Giannakis join the show HR 3: Dr. Wolfram Goessling, Andrew Wagner, Olivia, Brittany, Joshua, and Owen Kazanjian, Hunter Henry, and Howes Products join the show HR 4: Greg, Alma, Emilia, and Daniel Sarantopoulos, Daniel Sentana Lledo, and Will Flemming join the show

Bruins CEO Charlie Jacobs joins on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon. Jacobs talks about new Bruins Head Coach Marco Sturm and how the team wants to reinvent their identity in 2025.

Former Red Sox utility man and Co-Chair of The Jimmy Fund Brock Holt joins the show. Holt says he is still growing in his new position, but he loves the city of Boston and has seen the impact The Jimmy Fund has firsthand. He breaks down his favorite moments in Boston, and more.

Roman, Steven, and Mila Capraro, Lisa Scherber, Frank Martin, and Mike Thomas join the show on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon.

Frank Martin explains how his battle with colon cancer inspired him to get involved with The Jimmy Fund.

Trot Nixon felt the impact of The Jimmy Fund throughout his time with the Red Sox. He is grateful for the support from The Jimmy Fund and Dana-Farber as his father battles with cancer. He also feels something in the air with the 2025 Red Sox.

Taylor, Jen, and Andrew Laroche, Hadley, Matt, Jessica, and Cameron Kemmenoe, Vinny Del Negro, and Jacob Sands join the show on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon

Fitzy sits down with Vinny Del Negro who breaks down Dana-Farber's impact on his family after his mother was diagnosed with small cell lung cancer.

Derek Aube, Nadine Jackson, Charlie Jacobs, Brock Holt, James "Jim" Cichy, and Paul Richardson join on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon

Benjamin Ebert, Irene Ghobrial, and Trot and Kathryn Nixon join on Day One of the WEEI/NESN Jimmy Fund Radio-Telethon.

In this episode of the Oncology Brothers podcast, Drs. Rohit & Rahul Gosain welcome Dr. Jacob Sands, a thoracic medical oncologist from the Dana-Farber Cancer Institute, to discuss the recent FDA approval of Dato-DXD (datopotamab deruxtecan) for previously treated EGFR-mutated non-small cell lung cancer (NSCLC). Key Topics: •⁠  ⁠Overview of Dato-DXd and its FDA approval •⁠  ⁠Mechanism of action and study design of the TROPION Lung trials •⁠  ⁠Efficacy and safety profile of Dato-DXd •⁠  ⁠Management of side effects and clinical pearls •⁠  ⁠Treatment sequencing for EGFR-mutated NSCLC Join us as we dive into the details of the TROPION Lung trials that led to this significant approval, the mechanism of action of Dato-DXd, and the implications for patients with various EGFR mutations.  Dr. Sands shared insights on the study design, efficacy, and tolerability of this new antibody-drug conjugate, as well as important clinical pearls for managing side effects such as stomatitis, dry eyes, and interstitial lung disease (ILD). We also explored the current treatment landscape for EGFR-mutated NSCLC, including the sequencing of therapies and the potential role of Dato-DXd in clinical practice. Tune in for an informative discussion that highlights the exciting advancements in oncology and the hope they bring to patients. 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 like, subscribe, and check out our other episodes for more insights into the world of oncology!

Dr Jacob Sands from Dana-Farber Cancer Institute in Boston, Massachusetts, discusses recent developments with TROP2-directed antibody-drug conjugates in the management of non-small cell lung cancer. CME information and select publications here.

“At least some of the answer to these issues of compassion fatigue and burnout have to do making our practice environments the very, very best they can be so that nurses and other clinicians can really connect and care for patients in the ways that they want to be able to do that—and the patients need them to be able to do. I think there's a lot that is here already and will be coming, and I feel pretty optimistic about it,” ONS member Anne Gross, PhD, RN, NEA-BC, FAAN, senior vice president for patient care services and chief nursing officer at Dana-Farber Cancer Institute in Boston, MA, told ONS member Christine Ladd, MSN, RN, OCN®, NE-BC, member of the ONS 50th anniversary committee, during a conversation about burnout and compassion fatigue in oncology nursing. Ladd spoke with Gross and ONS member Tracy Gosselin, PhD, RN, NEA-BC, AOCN®, FAAN, senior vice president and chief nursing executive at Memorial Sloan Kettering Cancer Center in New York, NY, about the history of nurse well-being and how nurses and health systems are approaching it today. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0  Episode Notes  This episode is not eligible for NCPD.  ONS Podcast™ episodes: ONS 50th anniversary series Episode 315: Processing Grief as an Oncology Nurse Episode 292: What We Need to Do to Retain Today's Oncology Nursing Workforce Episode 291: Build a Sense of Belonging for Nurses and Patients Episode 264: Stop the Stressors and Improve Your Mental Health as a Nurse Episode 246: Create a Culture of Safety: Fair and Just Culture Episode 160: Build Innovative Staff Education Tools and Resources ONS Voice articles: Critical Event Debriefings Can Reduce Oncology Nurses' Risk of Compassion Fatigue and Burnout ONS Chapters and DNP Candidates Combine Forces to Support Oncology Nurse Well-Being Step Out of Reality With Virtual Breaks to Support Your Wellness at Work Clinical Journal of Oncology Nursing articles: Burnout and Well-Being: Evaluating Perceptions in Bone Marrow Transplantation Nurses Using a Mindfulness Application Engaging Nurse Residents Through Poetry Strategies to Mitigate Moral Distress in Oncology Nursing ONS Nurse Well-Being Learning Library ONS Communities ONS Chapters Connie Henke Yarbro Oncology Nursing History Center Oncology Nursing Foundation Resiliency Resources To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To find resources for creating an ONS Podcast club in your chapter or nursing community, visit the ONS Podcast Library. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From This Episode Gross: “I was on an oncology unit early in practice. And just like today, we were dealing with very sick patients. We were dealing with death and dying. We were administering very toxic treatments and really pushing a field forward in oncology. So there were similar challenges, but I think different from today. There weren't the kind of resources; there wasn't the body of work that's been done today around compassion fatigue and burnout, work-life balance, and things like that. There was not that body of literature and science like there is today. And so there was more of a grassroots kind of support building in the clinical environment that I think I experienced.” TS 2:35 Gosselin: “I think there's also a piece when we think about nurses in the work we do—we also have families. We have aging parents and children. And sometimes that burnout is multifactorial in that we have family obligations and other obligations that make it really hard. And for some people, they say work is their escape from some of that. Yet it's all hard to balance sometimes.” TS 8:09 Gosselin: “It's this question that people like Anne, myself, other chief nurses are saying. If we add this new technology, what are we going to take away? Do we need another alarm to ring to the phone or to their badge? How much can you ask people to do and not be distracted when they're at point of care delivering patient care? Technology should never be a distractor, nor should it tell us how to practice. The technologies we have today—I'm like, ‘Wow, I wish I had that when I started my career.' And yet there's also a double-edged sword to that. I think we have to balance when we think about care and care delivery.” TS 16:36 Gross: “There are so many resources, first of all, that ONS provides to all of us at all levels and in all points in our career and our path from novice to experts. And the needs, though, are the same. Whether you're a novice nurse or whether you're a very experienced nurse, you need to continue to learn and to get new information, and ONS is an incredible resource for that. … As I think both of us keep alluding to and emphasizing here, you also need that connection to other people. And that's what ONS provides—that opportunity to get connected to other people that might be working in some other part of the country or other part of the world but is dealing with similar things that you're dealing with. So it provides that opportunity, and then it also provides an opportunity to get involved. I think when you can get involved and be part of solving a problem, it doesn't then control you and you won't feel defeated by it.” TS 22:24

Dr. Sumanta (Monty) Pal and Dr. Kimmie Ng discuss the disturbing rise of early-onset gastrointestinal cancers, the unique challenges faced by younger patients, and key research that is shedding light on potential drivers of early diagnoses in colorectal cancer. TRANSCRIPT Dr. Sumanta (Monty) Pal: Hello, everyone. I'm Dr. Monty Pal, and I'm a medical oncologist and professor and vice chair of medical oncology at the City of Hope Comprehensive Cancer Center in Los Angeles. I'm really delighted to welcome you all to the ASCO Daily News Podcast as the show's new host. I'll be bringing you discussions with leaders in the oncology space on a variety of topics. I've been working hard with the ASCO team on picking the ideal topics to bring to you, and I'm really delighted to introduce my first guest, a dear friend, Dr. Kimmie Ng, to discuss this huge problem that we're seeing nowadays of early-onset GI cancers. Dr. Ng is the associate chief of the Division of Gastrointestinal Oncology at the Dana-Farber Cancer Institute, and she's an associate professor of medicine at Harvard Medical School in Boston. She serves as co-director of the Colon and Rectal Cancer Program. She's also the founding director of the Young-Onset Colorectal Cancer Center at Dana-Farber. I'm sure we'll talk a little bit about that today.  Just to note, our full disclosures are available in the transcript of this episode.  Dr Ng, it's so great to have you on the podcast. Thanks so much for joining us. Dr. Kimmie Ng: Thank you so much for having me. It's great to be here. Dr. Sumanta (Monty) Pal: I'm going to refer to you as Kimmie, if you don't mind, for the rest of the podcast here. Please, we'll go by first names, if you don't mind.  Your research has really done so much to help improve our understanding of early-onset GI cancers. You've done a lot of work to increase awareness in this space. I don't think there's a couple of months that passes by when I don't see you on television on Good Morning America or other shows really broadcasting this really critical message. I think there's a certain sensitivity that we all have to this issue, right? I mean, because receiving a cancer diagnosis at any age is very challenging, but I'm sure that young patients who face a colorectal cancer diagnosis have some very unique challenges. Could you give us a sense of some of those? Dr. Kimmie Ng: I think the other reason why so many people are interested in this and feel touched by this is that it's not just gastrointestinal cancers that are increasing in young people, but actually a multitude of different cancers have been rising in young individuals. And while it is difficult at any age to receive a cancer diagnosis, we do all know that young people getting a diagnosis like this do face unique challenges. Studies have shown that over 80% have children under the age of 18 when they are diagnosed with colorectal cancer, for example, under the age of 50. And many experience career and education disruptions. They are in what we call the ‘sandwich generation,' where they're not only taking care of young families or starting to think about starting a young family, but they're also taking care of elderly parents. So it's just a very busy stage of life, and to then be facing a usually terminal cancer diagnosis, it is extremely challenging. The other factors that we've seen that seem to be unique or more prevalent in young patients is that there are higher levels of psychosocial distress, depression, and anxiety, and a majority of patients do need medical attention and treatment for those things, whether it's medication treatment or whether it's counseling or support from psychosocial oncologists. And so the other big issue is fertility. We know that so many of the treatments that these young patients receive do permanently and negatively impact fertility. And for a person who is young, who may still be trying to expand their family or again start a family, it is very important that these young patients do receive counseling about fertility preservation prior to starting treatment. Dr. Sumanta (Monty) Pal: You know, it's so interesting you bring this up, and I think about a patient who's in their 40s diagnosed with this disease. They're in the same demographic as I am, as you are. You know, I'm 44 years old, and you know, I'm thinking about my 11- and 12-year-old and my aging parents, right? I mean, the dilemmas that you highlighted are precisely what I'm facing in life, and it's so true, right? If I had to take my day-to-day and superimpose on that a colorectal cancer diagnosis, it would just be problematic in so many spheres, so many spheres. Dr. Kimmie Ng: Absolutely. And because we did think going into this, starting our Young-Onset Colorectal Cancer Center, that these patients will need unique supports, we did conduct a qualitative study and held some focus groups of young-onset colorectal cancer patients as well as their caregivers. And we really identified four primary themes that I think reflect a lot of the experience of patients with cancer, no matter what type of cancer when they're diagnosed young. And the first is the need, feeling overwhelmed by the healthcare system, and the need for patient navigation. As we know, a lot of these patients are previously healthy before they're facing this very serious diagnosis. The second is the need for peer-to-peer support, where they really value connecting with other young patients going through a similar experience. The third, we talked about already, the need for kind of formal psychosocial support in the form of psychosocial oncologists or psychiatrists or social workers. And the last is an interest in research. They are really very invested in getting germline genetic testing as well as somatic genomic profiling to help guide their therapy. Dr. Sumanta (Monty) Pal: That's really encouraging to hear that they themselves are interested in participating in research. I mean, obviously, that's a great way to move the field forward. I view your area of work here as being such a vexing problem because no matter what way you slice it, young-onset colorectal cancer still remains a relatively small proportion of all diagnoses. So how do you go about studying this phenomenon? I mean, it must be challenging to really sort of investigate underlying causes when ostensibly this is still a small piece of the pie. Dr. Kimmie Ng: That is such a great question and is one of the challenges me and my research team think about every single day. As you mentioned, one of the major barriers is that although these cancers are rising in young people, the absolute number of patients being diagnosed is still relatively small, and if it's going to take large scale epidemiologic studies to really understand, for example, what the dietary and lifestyle risk factors are, you need a considerable number of patients in order to have enough power to reach definitive conclusions.  And so this is where it is so important to collaborate. Any single institution is not going to see enough young-onset patients with colorectal cancer to be able to do this work on their own. And so I have really been intent on establishing an international prospective cohort study of patients with young-onset colorectal cancer so that we can increase the numbers of patients we partner with to try to answer these questions, but also so that we can study this on a global scale, because unfortunately this is not something that's just plaguing the United States. It is actually happening in multiple countries around the world. So that is one barrier.  The second, I would say, is that we think it's early life exposures to whatever environmental factor it is that's causing the rise that is likely contributing the most. And so if you imagine how difficult it would be to start studying individuals from when they're children through adolescence, through adulthood, and then all the way until a cancer diagnosis is obtained, a study like that would take too long, would cost too much, and really wouldn't be feasible. So we need to think of alternative ways to really try and answer this question of what is driving this rise in young-onset colorectal cancer. Dr. Sumanta (Monty) Pal: Honestly, Kimmie, this seems like almost an unfair question in the context of what you just mentioned, the challenges in terms of ascertaining causality, right? I'll tell you, I cheated a little bit ahead of this podcast. Kimmie and I had dinner together in Los Angeles a couple months ago. She came out to deliver a Presidential Lectureship at City of Hope. We were delighted to have her. And we did have a couple of thoughts exchanged over potential drivers of these early diagnoses, leaning on perhaps one of the things that you and I are both interested in, the microbiome. But amongst all these things, vitamin D, microbiome, etc., and I won't hold you to this, do you have at least a general sense of what might be contributing to this early-onset phenomenon? Dr. Kimmie Ng: Yeah, as we talked about during my visit there to City of Hope, we do hypothesize that it is a complex interaction between our exposome, which is everything we are exposed to in our environment, which does include diet and lifestyle factors, interacting with host immunity and antitumor immunity, and as well as the microbiome and shaping the composition and diversity of the gut microbiome that are likely interacting to increase susceptibility to colorectal cancer at a younger age. And I will say one of the biggest discoveries, if you will, about what might be driving young-onset colorectal cancer was published a few months ago in Nature. And that paper identified a specific mutational signature caused by the genotoxin colibactin, which is often produced by an organism called pks+ E. coli, as being much more prevalent in younger patients with colorectal cancer than older patients. And so while it doesn't explain necessarily all of young-onset colorectal cancer and why it's rising, it does give us a clue that the microbiome is likely very important in perhaps why this is rising in young people. Dr. Sumanta (Monty) Pal: After you mentioned it, I went back and dove deep into that paper. I was fascinated, fascinated by the content there. And this is just a massive exploration across thousands of patients worldwide. So, I mean, if there is a way to get at least some hint of what's driving this phenomenon, I suppose that's it. So thank you for pointing me in the direction of that manuscript. Now that we've addressed the issue of diagnosis, if we could just, you know, verge on the topic of treatment, right? And this is something that I struggle with. When I have my young patients with kidney cancer, I don't know necessarily that my treatment paradigm changes a whole heck of a lot. I guess what I will say is I might be a little bit more aggressive about concepts like definitive management with surgery. I suppose perhaps their treatment tolerance is a little bit higher. But tell us about the setting of young-onset colorectal cancer. Is the philosophy any different in terms of the actual sort of management of these patients? Dr. Kimmie Ng: That's a great question, and actually I was honored to participate in the first international consensus guidelines group to try to come up with uniform recommendations for how to treat young patients with colorectal cancer. And you know, the overall consensus is just as you said, the medical care of these young patients right now is really not that much different than that of an older patient with colorectal cancer. There are a couple of distinctions. One is that all young patients should get germline genetic testing, given that there is a higher prevalence of pathogenic germline variants when you are diagnosed at a young age. And the second is what we've already talked about, which is that all young patients should be referred for counseling about fertility preservation prior to starting treatment. But otherwise, the chemotherapy regimens recommended, you know, surgery, radiation, all of that seems very similar to older patients. I will say that because most of our young patients with colorectal cancer are diagnosed with left-sided cancers, including rectal cancers, where some of the treatment may be morbid and result in lifelong complications, we do consider de-escalation of therapy and try to consider the long-term implications when it's safe to do so and won't compromise outcomes. The other concerning thing is that younger patients don't necessarily have a better prognosis than older patients. And multiple studies have shown this, that even though we both often treat younger patients more aggressively – they more often receive multi-agent chemotherapy, and more often undergo surgery and radiation – their survival is not necessarily correspondingly better than an older patient with colorectal cancer. So that suggests to us that maybe these cancers are indeed biologically different and perhaps more aggressive or perhaps less responsive to treatment. And so that is some of the focus of our research too, to understand what is actually different about these cancers and how they respond to treatment. Dr. Sumanta (Monty) Pal: It's such a paradox, isn't it, right? Because you just brought this to my mind. I guess on the one hand, our younger patients may be able to tolerate perhaps a greater amount of chemotherapy, targeted therapy, etc. But you're absolutely right. I mean, they do sort of have these lingering issues with side effects that may persist for much longer than the 80- or 90-year-old that we're treating in the clinic. I mean, these tend to be sort of lifelong consequences and sequelae that they're dealing with. So that really does evolve to be a challenge. You've kind of changed my mindset there a little bit. Dr. Kimmie Ng: Yeah, I do think survivorship issues and long-term complications of therapy do need to be considered, especially for a young person who we hope will live a very, very long time. And so part of the work that our Young-Onset Colorectal Cancer Center is doing, we are participating in a pilot navigation study where we navigate patients to survivorship earlier than we typically would, perhaps, for an older patient. And that's so we can get a head start on addressing some of those potential complications of therapy and hopefully mitigate them so that they don't become an issue long term. Dr. Sumanta (Monty) Pal: Do you think there's a role for de-escalation studies formally in these young populations of patients? Dr. Kimmie Ng: I think de-escalation studies are important overall, and specifically for locally advanced rectal cancer, which again is one of the most common types of colorectal cancer diagnosed in our young patients, there are certain populations that may be able to forgo the radiation treatment to the pelvis, for example, and there's more and more patients who now may become candidates for non-operative management where they may not necessarily need to have their rectal cancer surgically removed. And elimination potentially of both of those modalities of treatment can really avoid some of the most serious and morbid complications that often occur with these treatments. Dr. Sumanta (Monty) Pal: Really interesting. Now, this is not and will never be a political podcast, but you know, obviously we're dealing with the consequences of changes on funding and so forth that have evolved over time. And I think it's worth sort of speculating how the landscape of research may change on account of that. Could you comment perhaps a little bit on how some of the funding cuts that we've seen recently at the NIH might affect the body of work that you're so integrally involved in? Dr. Kimmie Ng: I am honestly very worried about the current funding environment. Colorectal cancer is the third most commonly diagnosed cancer among men and women in the United States and globally, and when you combine men and women together, the second leading cause of cancer death. But proportionally, we receive much less funding for colorectal cancer compared to other cancer types. And my thoughts have always been that perhaps this is because there is this stigma around colorectal cancer and maybe some of the symptoms associated with colorectal cancer. And so on top of that, to have additional challenges in obtaining funding, I worry what it will do to the pace of progress for especially young patients with this disease. Also, because of some new stipulations that perhaps international collaborations are being discouraged, I also worry about that aspect of it because young-onset colorectal cancer and gastrointestinal cancers in general is a global phenomenon happening in multiple countries around the world. And if we are to understand what the environmental factors are affecting the different rates of rise in these different countries, we do so much need that international collaboration. So yes, I am worried, and I do hope that conversations like this will spark an awareness of the need for more funding and continued funding into this disease. Dr. Sumanta (Monty) Pal: I will say that, and the audience can't see this because this is an audio program, but I'm wearing my Southwest Oncology shirt here, a SWOG, and it's one of the National Cancer Institute-funded cooperative groups. And you know, I was recently dismayed to find that, you know, funding got cut for international collaborations and enrollment in South America and Latin America. And this was traditionally actually a mainstay of our enrollment for many trials, including trials in rare cancers that present themselves in younger patients in the GU space. So, I completely agree with you. We've got to do something to address this funding issue to make sure that this body of work, both yours and mine, continues, without a doubt. Kimmie, this has been a delightful conversation. I really want to thank you for, you know, leading the charge in the young-onset colorectal cancer space, and you've done so much tremendous work here. Dr. Kimmie Ng: Thank you for having me. Dr. Sumanta (Monty) Pal: If you value the insights that you hear on the ASCO Daily News Podcast, please rate, review, and subscribe wherever you get your podcasts. And again, thank you for joining us today. 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. Find out more about today's speakers:   Dr. Sumanta (Monty) Pal @montypal Dr. Kimmie Ng @KimmieNgMD Follow ASCO on social media:    @ASCO on Twitter   ASCO on Bluesky  ASCO on Facebook    ASCO on LinkedIn    Disclosures:   Dr. Sumanta (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. Kimmie Ng: Honoraria: Seagen, GlaxoSmithKline Consulting or Advisory Role: CytomX Therapeutics, Jazz Pharmaceuticals, Revolution Medicines, Abbvie, Bayer, Pfizer, Agenus, Johnson & Johnson/Janssen, Etiome, AstraZeneca Research Funding (Inst.): Pharmavite, Janssen Other Relationship: JAMA

It's been a decade since PJ Branco's testicular cancer diagnosis in 2015. In early August 2025, he completed his third year as a participant in the PanMassChallenge⁩ with his personal goal to raise $10,000 for the Dana-Farber Cancer Institute. The two-day race covers 186 miles, and PJ is one of 1,000 living proof cyclists and volunteers who have been previously or are currently being treated for cancer. All the money raised in this charity event goes directly to cancer care at this treatment center.PJ was the third member of his family to survive cancer. His mom learned she had breast cancer in 2005, and his father received his colon cancer diagnosis a few years later when PJ was in college. In 2015, PJ had his right testicle removed, and three months later, when a scan showed an inflamed lymph node in his back, he underwent chemotherapy. He compares his cycling stamina in 2025 to a time during 2015. After the removal of his right testicle and chemotherapy, PJ considered it an accomplishment to walk up and down his driveway. Now, 10 years later, he talks about life with his wife and four-year-old son, and his dedication to giving back to the cancer institute that treated him and his mother. As he explained in the podcast, "I now give back to those who helped save my life." He shares his story in this episode of Don't Give Up on Testicular Cancer from the Max Mallory Foundation.  Send us a textSupport the showFind us on Twitter, Instagram, Facebook & Linkedin. If you can please support our nonprofit through Patreon.

i3 Health recently launched an exciting new online educational activity, “What's New with HER2: Charting New Paths in NSCLC Care.” This two-part series dives deep into the evolving role of HER2 in non–small cell lung cancer (NSCLC). In a special interview, Dr. Julia Kathleen Rotow—Clinical Director of the Lowe Center for Thoracic Oncology at Dana-Farber Cancer Institute and Assistant Professor of Medicine at Harvard Medical School—shares the latest breakthroughs in treating HER2-mutated NSCLC. She highlights why ongoing medical education is crucial in this fast-changing field and offers her insights on where HER2-targeted therapies are headed next. Stay tuned after the interview to listen to Module 1 of this accredited activity! Click below to complete the claim your CE credit: Module 1: https://bit.ly/49NCaQu Click below to complete the next Module in this series, Current and Emerging Treatments for HER2-Mutated NSCLC Module 2: https://bit.ly/405xEJO

i3 Health recently launched an exciting new online educational activity, “What's New with HER2: Charting New Paths in NSCLC Care.” This two-part series dives deep into the evolving role of HER2 in non–small cell lung cancer (NSCLC). In a special interview, Dr. Julia Kathleen Rotow—Clinical Director of the Lowe Center for Thoracic Oncology at Dana-Farber Cancer Institute and Assistant Professor of Medicine at Harvard Medical School—shares the latest breakthroughs in treating HER2-mutated NSCLC. She highlights why ongoing medical education is crucial in this fast-changing field and offers her insights on where HER2-targeted therapies are headed next. Stay tuned after the interview to listen to Module 1 of this accredited activity! Click below to complete the claim your CE credit: Module 2: https://bit.ly/405xEJO Click below to complete the Module 1 from this series, HER2 in NSCLC: Actionable Insights and Testing Recommendations Module 1: https://bit.ly/49NCaQu

In a discussion with CancerNetwork®, Jacob Sands, MD, assistant professor of Medicine at Harvard Medical School, thoracic oncologist at the Dana-Farber Cancer Institute, and investigator of the phase 2 TROPION-Lung05 trial (NCT04484142) and phase 3 TROPION-Lung01 trial (NCT04656652), which supported the accelerated approval of datopotamab deruxtecan-dlnk (dato-DXd; Datroway) in pretreated EGFR-mutant metastatic NSCLC in June 2025, discussed safety and efficacy considerations for the agent's use.1-3 He began by outlining a combined cohort of the TROPION-Lung05 and TROPION-Lung01 trials, which collectively showed an efficacy benefit with dato-DXd in patients with EGFR-mutant disease vs docetaxel. In the combined cohort, the median progression-free survival with dato-DXd reached 5.8 months, and the median overall survival was 15.6 months. Additional efficacy data revealed an objective response rate of 45% (95% CI, 35%-54%) and a median duration of response of 6.5 months (95% CI, 4.2-8.4).  Furthermore, Sands highlighted the most common toxicities observed with dato-DXd in this population, which included stomatitis, interstitial lung disease (ILD), and ocular toxicities. He also reviewed management strategies to mitigate their incidence and severity. Specifically, remedies include prophylaxis, oral hygiene, and dose reductions for stomatitis; using preservative-free eye drops and ophthalmology visits for ocular toxicity management and prevention; and monitoring for any incidence of high-grade ILD. He then touched upon next steps for research in this disease state, including the phase 2 ORCHARD trial (NCT03944772) evaluating dato-DXd with osimertinib (Tagrisso) in the second-line setting after progression on osimertinib and the phase 3 TROPION-Lung15 trial (NCT06417814), which is evaluating chemotherapy vs dato-DXd alone or with osimertinib.4,5 Sands concluded by discussing the implications for toxicity management in patients who experience responses that exceed median outcomes, suggesting that the toxicity profile may be more severe for this group. Emphasizing the broadness of outcomes with any drug, he expressed that patients with experiences that deviate from the observed median outcome are an important consideration for clinical practice. References Sands J, Ahn MJ, Lisberg A, et al. Datopotamab deruxtecan in advanced or metastatic non-small cell lung cancer with actionable genomic alterations: results from the phase II TROPION-Lung05 study. J Clin Oncol. Published online January 6, 2025. doi:10.1200/JCO-24-01349 Ahn MJ, Tanaka K, Paz-Ares L, et al. Datopotamab deruxtecan versus docetaxel for previously treated advanced or metastatic non-small cell lung cancer: the randomized, open-label phase III TROPION-Lung01 study. J Clin Oncol. Published online September 9, 2024. doi:10.1200/JCO-24-01544  FDA grants accelerated approval to datopotamab deruxtecan-dlnk for EGFR-mutated non-small cell lung cancer. News release. FDA. June 23, 2025. Accessed July 29, 2025. https://tinyurl.com/mtay7ab9 Yu HA, Goldberg SB, Le X, et al. Biomarker-directed phase II platform study in patients with EGFR sensitizing mutation-positive advanced/metastatic non-small cell lung cancer whose disease has progressed on first-line osimertinib therapy (ORCHARD). Clin Lung Cancer. 2021;22(6):601-606. doi:10.1016/j.cllc.2021.06.006 A study to investigate the efficacy and safety of dato-DXd with or without osimertinib compared with platinum based doublet chemotherapy in participants with EGFR-mutated locally advanced or metastatic non-small cell lung cancer (TROPION-Lung15). ClinicalTrials.gov. Updated July 16, 2025. Accessed July 29, 2025. https://tinyurl.com/56z3dmsp

Prof Susana Banerjee from The Institute of Cancer Research in London and Dr Ursula Matulonis from Dana-Farber Cancer Institute in Boston discuss important efficacy and safety data from the past year related to the management of ovarian, endometrial and cervical cancers.CME information and select publications here.

Hear Christopher McKim's journey with moderate to severe plaque psoriasis and the latest clinical trial results from dermatologist, Dr. Christine Cornejo. Join this discussion with moderator Archie Franklin as Christopher McKim, a BMS employee living with moderate to severe plaque psoriasis, and Dr. Christine Cornejo, Director and US Medical Engagement Lead for Dermatology and Rheumatology at BMS, offer a patient and physician's perspective on treating plaque psoriasis from the inside. Listen as Chris presents his journey along with Dr. Cornejo addressing effectiveness and safety information with clinical trial results for a prescription oral treatment option. The intent of this episode is to encourage those who have moderate to severe plaque psoriasis to work with their health care provider to find a treatment option that is right for them. This episode is sponsored by Bristol Myers Squibb. For more information view Full Prescribing Information and Medication Guide . ·       (0:00)   Intro to Psoriasis Uncovered and guest welcome to Bristol Myers Squibb employee and patient Christopher McKim and Dr. Christine Cornejo, Director and US Medical Engagement Lead for Dermatology and Rheumatology at Bristol Myers Squibb. ·       (2:15)  Where the journey to finding the right treatment option for Chris and his moderate to severe plaque psoriasis began.  ·       (3:09)   The decision by Chris and his provider to try an oral systemic medication. ·       (3:28)  The effects and impact of an oral systemic treatment for Chris and his plaque psoriasis. ·       (4:09)   Dr. Cornejo addresses efficacy and clinical trials results. ·       (5:58)   Common side effects and safety concerns for the treatment Chris and his health care provider decided to try.   ·       (6:28)   Health considerations patients and providers should discuss prior to using a systemic treatment.    ·       (6:54)   What to do should side effects occur. ·       (7:10)   How Chris feels with clearer skin after making a change in treatment. ·       (8:14)   Indication and Important Safety Information. Key Takeaways: ·       Moderate to severe plaque psoriasis is a systemic disease.    ·       If you're ready to treat from the inside there is a treatment option that may help.   ·       Work with a health care provider to find the right treatment for moderate to severe plaque psoriasis.   ·       Be proactive by taking steps to learn about treatment options including effectiveness, side effects, safety concerns, and what should be discussed with a health care provider before beginning a new treatment for plaque psoriasis.  Guest Bios:   Christopher (Chris) McKim joined BMS in June of 2022. In his current role he is a Regional Marketer for the dermatology division, prior to that he provided support for 9 Therapeutic Area Specialists for the Pacific South District in the GI division.  Prior to joining BMS, Chris worked at Sanofi, J&J, Leo Pharma, and Sun Pharma in various field and home office roles. Chris resides in beautiful San Diego with his family Susan (wife), Morgan 18, Maddy 16, Mason 14 and two Golden Retrievers and enjoys traveling, cooking and anything associated with the ocean (Deep Sea Fishing, S.C.U.B.A. diving, snorkeling, and boogie boarding). Dr. Christine Cornejo joined Bristol Myers Squibb in 2024 as Director, Medical Engagement Lead for Dermatology and Rheumatology. Prior to joining BMS, she practiced dermatology at Brigham and Women's Hospital and Dana-Farber Cancer Institute in Boston, MA, where she specialized in melanoma and high-risk skin cancer management and served as the Director of Confocal Microscopy. She also served as an Instructor at Harvard Medical School and led the Immunology and Infectious Diseases course for 1st year medical students. Resources: Current Oral Systemic Treatments For additional questions about treatment options contact the NPF Patient Navigation Center

In this JCO Article Insights episode, Michael Hughes summarizes “International Myeloma Society and International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma" by Avet-Loiseau et al. published on June 09, 2025 along with an interview with author Dr Nikhil C. Munshi, MD. TRANSCRIPT Michael Hughes: Welcome to this episode of JCO Article Insights. This is Michael Hughes, JCO's editorial fellow. Today I am interviewing Dr. Nikhil Munshi on the “International Myeloma Society and International Myeloma Working Group Consensus Recommendations on the Definition of High-Risk Multiple Myeloma” by Avet-Loiseau et al. At the time of this recording, our guest has disclosures that will be linked in the transcript. While some patients with multiple myeloma live for decades after treatment, others exhibit refractory or rapidly relapsing disease irrespective of treatment administered. We term this “high-risk myeloma.” Multiple risk stratification systems have been created, starting with the Durie-Salmon system in 1975 and evolving with the advent of novel therapeutics and novel treatment approaches. In 2015, the Revised International Staging System (R-ISS) was introduced, which incorporated novel clinical and cytogenetic markers and remained, until recently, a mainstay of risk stratification in newly diagnosed disease. Myeloma as a field has, just in the past few years, though, undergone explosive changes. In particular, we have seen groundbreaking advances not only in treatments - the introduction of anti-CD38 agents and the advent of cellular and bispecific therapies - but also in diagnostic technology and our understanding of the genetic lesions in myeloma. This has led to the proliferation of numerous trials employing different definitions of high-risk myeloma, a burgeoning problem for patients and providers alike, and has prompted attempts to consolidate definitions and terminology. Regarding cytogenetic lesions, at least, Kaiser et al's federated meta-analysis of 24 therapeutic trials, published here in the JCO in February of 2025 and recently podcasted in an interview with associate editor Dr. Suzanne Lentzsch, posited a new cytogenetic classification system to realize a shared platform upon which we might contextualize those trial results. This article we have here by Dr. Avet-Loiseau, Dr. Munshi, and colleagues, published online in early June of this year and hot off the presses, is the definitive joint statement from the International Myeloma Society (IMS) and the International Myeloma Working Group (IMWG). What is high-risk multiple myeloma for the modern era? The IMS and IMWG Genomics Workshop was held in July 2023 and was attended by international myeloma experts, collaborating to reach consensus based on large volumes of data presented and shared. The datasets included cohorts from the Intergroupe Francophone du Myélome (IFM); the HARMONY project, comprised of multiple European academic trials; the FORTE study, findings from which solidified KRd as a viable induction regimen; the Grupo Español de Mieloma Múltiple (GEM) and the PETHEMA Foundation; the German-Speaking Myeloma Multicenter Group (GMMG); the UK-based Myeloma XI, findings from which confirmed the concept of lenalidomide maintenance; Emory 1000, a large, real-world dataset from Emory University in Atlanta; the Multiple Myeloma Research Foundation Clinical Outcomes in Multiple Myeloma to Personal Assessment of Genetic Profile (CoMMpass) dataset; and some newly diagnosed myeloma cohorts from the Mayo Clinic. Data were not pooled for analyses and were assessed individually - that is to say, with clear a priori understanding of whence the data had been gathered and for what original purposes. Consensus on topics was developed based on the preponderance of data across studies and cohorts. In terms of results, substantial revisions were made to the genomic staging of high-risk multiple myeloma, and these can be sorted into three major categories: A) alterations to the tumor suppressor gene TP53; B) translocations involving chromosome 14: t(14;16) (c-MAF overexpression), t(14;20) (MAFB overexpression), and t(4;14) (NSD2 overexpression); and C) chromosome 1 abnormalities: deletions of 1p or additional copies of 1q. In terms of category A, TP53 alterations: Deletion of 17p is present in up to 10% of patients at diagnosis and is enriched in relapsed or refractory disease. This is well-documented as a high-risk feature, but the proportion of the myeloma cells with deletion 17p actually impacts prognosis. GEM and HARMONY data analyses confirmed the use of 20% clonal cell fraction as the optimal threshold value for high-risk disease. That is to say, there must be the deletion of 17p in at least 20% of the myeloma cells on a FISH-analysis of a CD138-enriched bone marrow sample to qualify as high-risk disease. TP53 mutations can also occur. Inactivating mutations appear to have deleterious effects similar to chromosomal losses, and the biallelic loss of TP53, however it occurs, portends particularly poor prognosis. This effect is seen across Myeloma XI, CoMMpass, and IFM cohorts. Biallelic loss is rare, it appears to occur in only about 5% of patients, but next-generation sequencing is nevertheless recommended in all myeloma patients. Category B, chromosome 14 translocations: Translocation t(14;16) occurs in about 2% to 3% of patients with newly diagnosed disease. In the available data, primarily real-world IFM data, t(14;16) almost always occurs with chromosome 1 abnormalities. Translocation t(4;14) occurs in about 10% to 12% of newly diagnosed disease, but only patients with specific NSD2 alterations are, in fact, at risk of worse prognosis, which clinically appears to be about one in every three of those patients. And so together, the CoMMpass and Myeloma XI data suggest that translocation t(4;14) only in combination with deletion 1p or gain or amplification of 1q correlates with worse prognosis. Translocation t(14;20) occurs in only 2% of newly diagnosed disease. Similar to translocation t(4;14), it doesn't appear to have an effect on prognosis, except if the translocation co-occurs with chromosome 1 lesions, in which case patients do fare worse. Overall, these three translocations - t(14;16), t(4;14), and t(14;20) - should be considered high-risk only if chromosome 1 aberrations are also present. In terms of those chromosome 1 aberrations, category C, first deletions of 1p: Occurring in about 13% to 15% of newly diagnosed disease, deletion 1p eliminates critical cell checkpoints and normal apoptotic signaling. In the IFM and CoMMpass dataset analyses, biallelic deletion of 1p and monoallelic deletion of 1p co-occurring with additional copies of 1q denote high-risk. In terms of the other aberration in chromosome 1 possible in myeloma, gain or amplification of 1q: This occurs in up to 35% to 37% of newly diagnosed disease. It upregulates CKS1B, which is a cyclin-dependent kinase, and ANP32E, a histone acetyltransferase inhibitor. GEM and IFM data suggest that gain or amplification of 1q - there was no clear survival detriment to amplification - is best considered as a high-risk feature only in combination with the other risk factors as above. Now, in terms of any other criteria for high-risk disease, there remains one other item, and that has to do with tumor burden. There has been a consensus shift, really, in both the IMS and IMWG to attempt to develop a definition of high-risk disease which is based on biologic features rather than empirically observed and potentially temporally dynamic features, such as lactate dehydrogenase. Beta-2 microglobulin remains an independent high-risk indicator, but care must be taken when measuring it, as renal dysfunction can artificially inflate peripheral titers. The consensus conclusion was that a beta-2 microglobulin of at least 5.5 without renal failure should be considered high-risk but should not preclude detailed genomic profiling. So, in conclusion, the novel 2025 IMS-IMWG risk stratification system for myeloma is binary. It's either high-risk disease or standard-risk disease. It's got four criteria. Number one, deletion 17p and/or a TP53 mutation. Clonal cell fraction cut-off, remember, is 20%. Or number two, an IGH translocation - t(4;14), t(14;16), t(14;20) - with 1q gain and/or deletion of 1p. Or a monoallelic deletion of 1p with 1q additional copies or a biallelic deletion of 1p. Or a beta-2 microglobulin of at least 5.5 only when the creatinine is normal. This is a field-defining work that draws on analyses from across the world to put forward a dominant definition of high-risk disease and introduces a new era of biologically informed risk assessment in myeloma. Now, how does this change our clinical approach? FISH must be performed on CD138-enriched samples and should be performed for all patients. Next-generation sequencing should also be performed on all patients. Trials will hopefully now begin to include this novel definition of high-risk multiple myeloma. It does remain to be seen how data from novel therapeutic trials, if stratified according to this novel definition, will be interpreted. Will we find that therapies being evaluated at present have differential effects on myelomas with different genetic lesions? Other unanswered questions also exist. How do we go about integrating this into academic and then community clinical practice? How do we devise public health interventions for low-resource settings? To discuss this piece further, we welcome the esteemed Dr. Nikhil Munshi to the podcast. Dr. Munshi is a world-renowned leader in multiple myeloma and the corresponding author on this paper. As Professor of Medicine at Harvard Medical School, Director of the Multiple Myeloma Effector Cell Therapy Unit, and Director of Basic and Correlative Science at the Jerome Lipper Multiple Myeloma Center of the Dana-Farber Cancer Institute, he has presided over critical discoveries in the field.  Thank you for joining us, Dr. Munshi. Dr. Nikhil Munshi: Oh, it's my pleasure being here, Michael, to discuss this interesting and important publication. Michael Hughes: I had a few questions for you. So number one, this is a comprehensive, shall we say, monumental and wide-ranging definition for high-risk myeloma. How do you hope this will influence or impact the ways we discuss myeloma with patients in the exam room? And how do we make some of these components recommended, in particular next-generation sequencing, feasible in lower-resource settings? Dr. Nikhil Munshi: So those are two very important questions. Let's start with the first: How do we utilize this in our day-to-day patient care setting? So, as you know well, we have always tried to identify those patients who do not do so well with the current existing treatment. And for the last 30 years, what constitutes a myeloma of higher risk has continued to change with improvement in our treatment. The current definition basically centers around a quarter of the patients whose PFS is less than 2 to 3 years. And those would require some more involved therapeutic management. So that was a starting point of defining patients and the features. As we developed this consensus amongst ourselves - and it's titled as “International Myeloma Society, International Myeloma Working Group Consensus Recommendation” - this IMS-IMWG type of recommendation we have done for many years, improvising in various areas of myeloma care. Now, here, we looked at the data that was existing all across the globe, utilizing newer treatment and trying to identify that with these four-drug regimens, with transplant and some of the immunotherapy, which group of patients do not do as well. And this is where this current algorithm comes up. So before I answer your question straight, “How do we use it?” I might like to just suggest, “What are those features that we have identified?” There are four features which constitute high-risk disease in the newer definition. Those with deletion 17p with 20% clonality and/or TP53 mutation. Number two, patients with one of the translocations - t(4;14), t(14;16), or t(14;20) - co-occurring with 1q amplification or deletion 1p32. And that's a change. Previously, just the translocation was considered high-risk. Now we need a co-occurrence for it to be called high-risk. The third group is patients having biallelic deletion 1p32 or monoallelic deletion 1p32 along with 1q amplification. And finally, patients with high beta-2 microglobulin, more than or equal to 5.5 mg/dL, with normal creatinine less than 1.2 mg/dL. And the question, “How do we use this?” There are multiple areas where we incorporate high-risk features in our treatment algorithm. One of the first areas is where we would consider the induction regimen. If a patient has a high-risk disease, we would definitely consider a four-drug regimen rather than a three-drug regimen, although we are beginning to incorporate four-drug for all groups. That's one important thing. Number two, those are the patients where we do consider consolidation with transplant or maybe in the new world, considering some of the immunotherapeutic consolidation more early or more aggressively. Number three, these are the patients who get a little bit more maintenance therapy. So normally, lenalidomide might end up being our standard maintenance regimen. In patients who have high-risk disease, we incorporate either addition of daratumumab or the anti-CD38 targeting antibody and/or addition of proteasome inhibitor, either bortezomib or carfilzomib. So you would have multi-drug maintenance therapy in these patients. And in high-risk patients, we follow them with maintenance longer periods of time. One very critically important point to keep in mind is that to get the better outcome in high-risk disease, we must try to get them into MRD negativity because there is clear data that patients who do achieve MRD negativity, despite having high-risk disease, have a much superior outcome. They become near to standard-risk disease. And so, in high-risk patients, I would try to do whatever various options I have to try and get them into MRD-negative status. And when these patients relapse, we do not wait for the classic progression criteria to be met before we intervene. We would propose and suggest that we intervene earlier before the disease really blasts off. And so there are a number of areas in our setting where this high-risk definition will help us intervene appropriately and also with appropriate aggressiveness to achieve better outcome, to make this similar to standard-risk disease. Michael Hughes: Thank you, Dr. Munshi. And thoughts on how to really integrate this not only into academic centers but also lower-resource settings? Dr. Nikhil Munshi: So that's a very important question, Michael. And when we were developing this consensus, we were very cognizant of that fact. So wherever available, I think we are recommending that over a period of next 2, 3, 5 years, we should begin to switch over to sequencing-based methods because two components of this definition, one is TP53 mutation, which we cannot do without sequencing, and also reliably detecting deletion 1p requires sequencing-based method. So in the low-resource countries - and there are many in this world, and also even in our own country, patients may not be able to afford it - the older method with FISH or similar such technology, which is more affordable, is also acceptable for current time. They may miss a very small number of patients, maybe 2% to 3%, where these finer changes are not picked up, but a majority of this would be captured by them. So the current practice might still be applicable with some limitation in those patient populations, and that's what we would recommend. What is happening, fortunately, is that actually sequencing-based method is becoming cheaper. And in many centers, it is cheaper to do the sequencing rather than to do the FISH analysis. And so my hope is that even in low-resource centers, sequencing might be more economical in the end. It's, I think, the access to technology, which is a little bit limited currently, but it's hopefully becoming available soon. Michael Hughes: Thank you, Dr. Munshi. And staying for a minute and looking at the multiple myeloma subsets which might be missed by this really still very broad-ranging high-risk definition, at least by prior risk stratification systems, right, there is this group of patients who have standard-risk cytogenetics by R-ISS or R2-ISS, but they have primary refractory disease or they relapse early. We call these, as you are well aware, functionally high-risk disease. What proportion of previously FHR, functionally high-risk, myeloma patients do you expect to be captured by this novel definition? Dr. Nikhil Munshi: So I think the newer definition - and we can look at it both ways, but the newer definition should capture most of the functionally high-risk definition. To put it differently, Michael, there are patients who we know are, as you mentioned, functionally high-risk. Those are the patients who might have plasma cell leukemia, those who might have extramedullary disease, those who might not respond to our four-drug induction. If you don't respond to the four-drug induction, almost by definition, they are high-risk. However, a majority of them have one of the abnormalities that we are describing here. There would be a very small proportion which may not have. And if they do not have, we know one of the important components of this definition here is also that the genome, we know, keeps on evolving. So there may be a very small clone with the high-risk feature which was not obvious in the beginning. Following treatments or following relapse, that clone predominates, and now the patient's disease becomes high-risk.  So the definition would incorporate or would capture these functional high-risk patients, but as you said, in countries where resources are not available, using this functional high-risk would also be helpful and advantageous. Sometimes LDH ends up being a high-risk. In our studies, LDH has not come out to be high-risk anymore because the features we are describing captures most of those patients, but those alternatives, older, can still be considered if other newer techniques are not available. Michael Hughes: Got you. And in terms of these older definitions, yes, that incorporate tumor burden, these empirical observations about how myeloma presents, do you foresee any additional tumor burden indicators being added to future definitions of high-risk disease? Or do you instead see this particular definition as a major waypoint on the journey towards a fully biologically grounded definition of high-risk disease? Dr. Nikhil Munshi: I think your second part is what is going to happen. I think the tumor burden-related definition is being now replaced by the biological or genomic-based definition. And I think at some point, it will be quite fully replaced. One component not here, and it is because one thing, we don't have enough data; number two, we don't know how it will pan out, is also the influence of the microenvironment on the risk definition. For example, the immune system, the immune function, etc. But not enough data exists to suggest how it would change the current definition. So in future, would a definition be totally genomic or it could be more integrative? And my personal guess is that it would be more integrative and that some immune features might come into the picture, especially now that we are using immune-based therapy as a very important component of treatment - CAR T-cells, bispecific, and antibody-based treatments. What role the immune system plays in either supporting tumor or what role suppression of the anti-tumor immunity plays? They all will be important how patient outcomes end up being, and which in turn could translate into how patient's risk stratification might happen. So I think the older tumor burden-related definitions probably will become things of the past. What we have currently proposed and consensus developed is the new path forward, and over time, some microenvironmental influences, if defined and found to be important, may get some more incorporation if it compares favorably with the genomic features. Michael Hughes: Thank you, Dr. Munshi for that enlightening response.  To conclude the podcast, I'd like to look to the future and to the immediate future, what are the next steps for high-risk disease definition between now and discussing an integrated genomic-microenvironment-based definition? Will we see attempts to refine? Will we see a multi-level system, things like this? Dr. Nikhil Munshi: Yeah, so I think the current definition will be here to stay for the next 10 years or so. I think this has been developed using a large amount of data, so we do believe that this will remain fine. It has been validated now within the last six months by a few of the other studies. So there won't be a quick change. But we will try to, all of us will try to innovate. And as you very rightly bring up, the areas of research would include looking at the expression or transcriptomic component. Does that matter? And we do believe a small number of patients will have transcriptomic changes, not looked at the DNA changes, and may play a role. There are newer components, so long non-coding RNA, for example, is going to be an important component to look at, how it impacts the disease outcome, etc. There are also some of the proteomic-related changes which may become important in our studies. And then as we discussed, microenvironment and immunological changes. So these are the future areas of ongoing research where we all should collect data, and then in the next 5 to 10 years, we'll have another group meeting to see has anything changed or any of the features have become more important.  Most of the time, some of the older features are lost because they are not as critically high-risk, and the newer features come in. And so the historical background for just one second, there was a time when chromosome 13 was considered a high-risk disease. We now don't even mention it because it's not high-risk. The newer treatments have improved the outcome. t(4;14) used to be a high-risk disease. Now by itself today, in this definition by itself is not; it needs to be with something else. And so I think this is a great sign of progress. As we improve the treatment and outcomes, some of the features will become less important, new features will come up, and we'll need to keep on evolving with time and with technology and make it better for patients. Michael Hughes: Thank you so much, Dr. Munshi, for your wisdom, for your sagacity, for your historical perspective as well.  Thank you for listening to JCO Article Insights. Please come back for more interviews and article summaries. And be sure to leave us a rating and review so others can find our show. For more podcasts and episodes from ASCO, please visit asco.org/podcasts. 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.  

At the 2025 Kidney Cancer Research Summit hosted by KidneyCAN, CancerNetwork® spoke with a variety of leading experts about key developments in the research and management of kidney cancer. Throughout the meeting, presenters shared their findings related to updated clinical trial results, personalized cancer vaccines, potential biomarkers of interest, and other advancements in the field. Thomas Powles, MBBS, MCRP, MD, discussed outcomes from a quality-adjusted survival time without symptoms or toxicity (Q-TWiST) analysis of the phase 3 LITESPARK-005 trial (NCT04195750), in which investigators evaluated treatment with belzutifan (Welireg) vs everolimus (Afinitor) among patients with advanced renal cell carcinoma (RCC). Powles, a professor of genitourinary oncology, lead for Solid Tumor Research, and director of Barts Cancer Institute at St. Bartholomew's Hospital, Queen Mary University of London, stated that these data demonstrate how belzutifan is more active and better tolerated than everolimus in this patient population. David A. Braun, MD, PhD, assistant professor at Yale School of Medicine and member of the Center of Molecular and Cellular Oncology within the Yale Cancer Center, detailed his presentation on a personalized neoantigen cancer vaccine as a treatment for those with RCC. Based on his presentation, Braun highlighted how neoantigen vaccines may effectively yield T-cell responses in patients, illustrating a need for additional, larger studies to elucidate the clinical activity of this modality in an adjuvant setting. Additionally, Wenxin (Vincent) Xu, MD, a medical oncologist at Dana-Farber Cancer Institute and an assistant professor of medicine at Harvard Medical School, spoke about his presentation on how kidney injury molecule-1 (KIM-1) may serve as a prognostic biomarker of response to therapy in patients with RCC. His research posed questions on how KIM-1 can inform the use of adjuvant therapy or specific therapeutic combinations like nivolumab (Opdivo) plus ipilimumab (Yervoy) for this patient population. Eric Jonasch, MD, gave an overview of his presentation focused on the Kidney Cancer Research Consortium, a research partnership spanning 7 institutions dedicated to facilitating mechanistic, hypothesis-testing clinical trials in RCC. Jonasch, a professor in the Department of Genitourinary Medical Oncology of the Division of Cancer Medicine at The University of Texas MD Anderson Cancer Center, described how this collaboration aims to link identifiable biological characteristics of RCC subtypes to specific treatment strategies while developing predictive biomarkers. KidneyCAN is a nonprofit organization with a mission to accelerate cures for kidney cancer through education, advocacy, and research funding. You can learn more about KidneyCAN's work here: https://kidneycan.org/ References 1. Powles T, de Velasco G, Choueiri TK, et al. Quality-adjusted time without symptoms or toxicity (Q-TWiST) analysis of belzutifan versus everolimus in previously treated advanced renal cell carcinoma (RCC): LITESPARK-005 (LS-005). Presented at the 2025 Kidney Cancer Research Summit; July 17-18, 2025; Boston, MA. Abstract 13. 2. Braun DA. Personalized vaccines in kidney cancer: a journey from concept to clinic. Presented at the 2025 Kidney Cancer Research Summit; July 17-18, 2025; Boston, MA. 3. Xu W. From bench to bedside: advancing KIM-1 as a tool for clinical decision-making. Presented at the 2025 Kidney Cancer Research Summit; July 17-18, 2025; Boston, MA. 4. Jonasch E. Building the infrastructure for discovery: a clinical trial consortium to accelerate kidney cancer research. Presented at the 2025 Kidney Cancer Research Summit; July 17-18, 2025; Boston, MA.

As research in dedifferentiated liposarcoma (DDLPS) continues to advance, the importance of multidisciplinary collaboration and access to innovative therapies remains at the forefront of patient care. Recently, Dr. Richard Riedel of Duke Cancer Institute and Dr. Candace Haddox of Dana-Farber Cancer Institute co-chaired i3 Health's DDLPS Task Force activity, which brought together a panel of experts to address the complexities of this rare and challenging sarcoma subtype. With new clinical trials underway and a growing understanding of the disease's molecular landscape, Dr. Riedel and Dr. Haddox sat down to highlight promising research directions and insights in honor of Sarcoma Awareness Month in July. After listening to the interview, stay tuned to hear the full accredited podcast with Dr. Riedel and Dr. Haddox, and click the link below to claim free CME/AAPA credit. Click the links below for the Task Force activity! - Accredited CME/AAPA Podcast: i3health.com/course-information/podcast-ddlps - Position Statement Published in Cancer Treatment Reviews: www.cancertreatmentreviews.com/article/S…/fulltext - Live Task Force Recording: youtu.be/Otr5_tiFQ68

Dr Ajay K Nooka from Winship Cancer Institute of Emory University in Atlanta, Georgia, and Dr Paul G Richardson from Dana-Farber Cancer Institute in Boston, Massachusetts, discuss recent updates on available and novel treatment strategies for multiple myeloma. CME information and select publications here.

Early-onset gastrointestinal cancers, typically defined as occurring in patients younger than age 50, are increasing worldwide. A recent JAMA Review summarizes current data on early-onset colorectal, pancreatic, and esophagogastric cancers. Coauthor Kimmie Ng, MD, MPH, of Dana-Farber Cancer Institute joins JAMA Deputy Editor Kristin Walter, MD, MS to discuss. Related Content: Early-Onset Gastrointestinal Cancers Screening for Helicobacter pylori to Prevent Gastric Cancer First-Line Sugemalimab Plus Chemotherapy for Advanced Gastric Cancer

What happens when cancer strikes in your 20s or 30s? How do you navigate life-changing diagnoses during the most formative years of your life? In this powerful episode of All Talk Oncology, Kenny Perkins speaks with Dr. Venkataraman, a young adult cancer specialist at Dana-Farber Cancer Institute, who is deeply committed to caring for patients with rare cancers like sarcoma. From the emotional trauma of delayed diagnoses to the complexities of survivorship, Dr. V shares how he supports patients not just through treatment—but through rediscovering their lives afterward. Key topics discussed: Why young adults are often diagnosed late—and what we can do about it How sarcoma differs from other cancers and why it's so misunderstood Treatment challenges: surgery, radiation, chemotherapy, and their impact Why survivorship care is just as important as treatment The mental health struggles cancer patients rarely talk about The role of personalized care: meeting patients where they are Advances in sarcoma research, clinical trials, and treatment protocols Empowering patients to take charge of their own journey Creative outlets for physicians: how Dr. V uses reflective writing to process the emotional weight of oncology   Immortalize your voice by being an ALL TALK ONCOLOGY GUEST! Just fill-out this FORM.   SOCIAL MEDIA LINKS: All Talk Oncology: Instagram & Facebook JOIN OUR FREE COMMUNITY: Facebook Community WEBSITE: https://www.alltalkoncology.com

In this inspiring episode of the Fathers of the Future Podcast, host Luke Kayyem sits down with his coaching client and friend, Jesse Mufasa Goldsmith, to discuss Jesse's remarkable transformation. Previously known as "Big Cat," a nickname tied to his 385-pound frame and party-heavy lifestyle, Jesse shares how he shed 135 pounds, embraced sobriety, and completed the Boston Marathon. The journey began 18 months ago after a serendipitous meeting with Luke on a golf course, followed by a pivotal moment of hitting rock bottom. Jesse's story highlights his shift from a self-destructive identity to one of resilience and purpose, embodied in his new persona, "Mufasa," inspired by his commitment to being a strong, protective father to his daughter, Sophie.Jesse recounts key milestones, including adopting intermittent fasting, quitting alcohol, and training for two half-marathons and the Boston Marathon, all while overcoming a relapse and battling physical and mental challenges. With Luke's guidance, Jesse rebuilt his confidence, rekindled his competitive drive as a commercial real estate broker, and inspired his family and colleagues. The episode culminates in Jesse's emotional Boston Marathon finish, a testament to his dedication and the support of his community, leaving listeners with a powerful message about transformation, legacy, and inspiring others.Guest: Jesse Mufasa Goldsmith, commercial real estate broker at Newmark, former college tennis player, and father to Sophie.Key Themes:Identity Shift: From "Big Cat," a persona tied to excess and self-destruction, to "Mufasa," symbolizing strength and protection for his daughter.Transformation Journey: Losing 135 pounds naturally, quitting alcohol, and completing the Boston Marathon.Rock Bottom Moment: A wake-up call during a daddy-daughter trip in Salt Lake City, leading to sobriety and commitment to change.Coaching Impact: Luke Kayyem's non-judgmental approach helped Jesse rebuild his life through small, consistent changes.Boston Marathon: Ran for the Dana-Farber Cancer Institute, raising $17,000, and finished in 5:27:55, just two minutes before the sweep.Highlights:Meeting Luke on a golf course in Flagstaff, facilitated by mutual friend Riyadh Naza.Overcoming a relapse during a golf trip, recommitting to sobriety and training.Emotional family reunion in Boston, with Jesse's parents, wife, and daughter supporting him.Upcoming documentary, Road to Boston, focusing on mental health awareness, set for release around July 4, 2025, on YouTube.Resources:Luke Kayyem's Website: https://www.lukekayyem.com/Schedule a Call with Luke: https://www.lukekayyem.com/scheduleLuke's Facebook: https://www.facebook.com/lukekayyemLuke's Instagram: https://www.instagram.com/lukekayyem

First-Line Therapy—Has the Standard of Care Shifted for Good?In this episode, Dr. Sara Tolaney, of Dana-Farber Cancer Institute, discusses how DESTINY-Breast09 is redefining first-line treatment in HER2-positive metastatic breast cancer. She explores whether T-DXd plus pertuzumab should replace the long-standing THP regimen, the future role of induction-maintenance strategies, and open questions on optimal therapy duration.   Let us know what you thought of this week's episode on Twitter: @physicianswkly Want to share your medical expertise, research, or unique experience in medicine on the PW podcast? Email us at editorial@physweekly.com! Thanks for listening!

Dr Jeremy Abramson from Massachusetts General Hospital in Boston, Dr Joshua Brody from the Tisch Cancer Institute in New York, New York, Dr Christopher Flowers from The University of Texas MD Anderson Cancer Center in Houston, Dr Ann LaCasce from Dana-Farber Cancer Institute in Boston, Massachusetts, and Dr Tycel Phillips from City of Hope Comprehensive Cancer Center in Duarte, California, discuss patient cases and provide their perspectives on clinical datasets informing the care of patients with non-Hodgkin lymphoma. CME information and select publications here.

In today's episode, supported by Bayer, we had the pleasure of speaking with Alicia Morgans, MD, MPH, and Neal Shore, MD, FACS, about the FDA approval of darolutamide (Nubeqa) plus androgen deprivation therapy for patients with metastatic castration-sensitive prostate cancer (mCSPC). Morgans is the medical director of the survivorship program at Dana-Farber Cancer Institute; as well as an associate professor of medicine at Harvard Medical School, both in Boston, Massachusetts. Shore is the medical director of the Carolina Urologic Research Center. In our exclusive interview, Drs Morgans and Shore discussed the significance of this approval; key efficacy, safety, and quality of life data from the pivotal phase 3 ARANOTE trial (NCT04736199); and how this regulatory decision both opens doors for the treatment of more patients and raises questions about the optimal role of darolutamide in the management of mCSPC. 

Kimmie Ng, MD, MPH, a JAMA associate editor and associate chief of the Division of Gastrointestinal Oncology at the Dana-Farber Cancer Institute, shares highlights from the American Society of Clinical Oncology's annual meeting, including new research on diet, exercise, and cancer survival and the best time of day for treatment. Related Content: Lifestyle and Cancer Survival, the Best Time of Day for Treatment, and More—Highlights From ASCO

In this episode, we speak with Chris Hadley, Managing Director at Berkshire Partners, a 100% employee-owned investor in private and public equity. The private equity team invests in well-positioned, growing companies across business & consumer services, healthcare, industrials, and technology & communications. Founded in 1986, Berkshire is currently investing from its Fund XI, which closed in 2024 with $7.8 billion in commitments. The firm has completed over 150 investments and is known for partnering closely with management teams to drive growth across market cycles. A leader within the firm's healthcare investment team, Chris has demonstrated exceptional leadership and strategic insight over his 27-year tenure. Known for his unique ability to build trust and foster collaboration, he has earned the respect of peers and portfolio company management teams alike, and was recognized by GrowthCap as a Top Healthcare Investor of 2025. Chris supports Dana-Farber Cancer Institute and McLean Hospital. I am your host, RJ Lumba. We hope you enjoy the show. If you like the episode, click to follow.

Dr Patrick Wen from the Dana-Farber Cancer Institute in Boston, Massachusetts, discusses the current and future management of IDH-mutant gliomas. CME information and select publications here.

Cedar Connell was 15 years old when he found himself on his way to Lurie Children's Hospital in Chicago to begin his treatment for B Cell Acute Lymphoblastic Leukemia in 2022. Cedar and his mom Kiki will talk about the difficult treatment that he went through, including his move from Chicago to the Dana Farber Cancer Institute in Boston in 2023. Cedar is now getting ready to do his part for the Leukemia and Lymphoma Society as TEAM CONNELLSLLS will be getting ready for a 31 day challenge beginning on July 1st and ending on August 1st to exercise 3 miles each day for that time period, in the hope that they raise 35,000.

In today's episode, supported by Coherus BioSciences, we had the pleasure of speaking with Michael Dennis, MD, about recent updates to the nasopharyngeal carcinoma treatment paradigm. Dr Dennis is a physician at Dana-Farber Cancer Institute; as well as an instructor in medicine at Harvard Medical School, both in Boston, Massachusetts. In our exclusive interview, Dr Dennis discussed the latest National Comprehensive Cancer Center guideline updates for the treatment of patients with nasopharyngeal carcinoma; practice-informing data from the phase 3 JUPITER-02 trial (NCT03581786), which investigated first-line toripalimab-tpzi (Loqtorzi) plus chemotherapy in patients with recurrent or metastatic nasopharyngeal carcinoma; and ongoing developments in the locally advanced treatment setting.

Dr. Allison Zibelli and Dr. Rebecca Shatsky discuss advances in breast cancer research that were presented at the 2025 ASCO Annual Meeting, including a potential new standard of care for HER2+ breast cancer, the future of ER+ breast cancer management, and innovations in triple negative breast cancer therapy. Transcript Dr. Allison Zibelli: Hello and welcome to the ASCO Daily News Podcast. I'm Dr. Allison Zibelli, your guest host of the podcast today. I'm an associate professor of medicine and a breast medical oncologist at the Sidney Kimmel Comprehensive Cancer Center at Jefferson Health. There was a substantial amount of exciting breast cancer data presented at the 2025 ASCO Annual Meeting, and I'm delighted to be joined by Dr. Rebecca Shatsky today to discuss some of these key advancements. Dr. Shatsky is an associate professor of medicine at UC San Diego and the head of breast medical oncology at the UC San Diego Health Moores Cancer Center, where she also serves as the director of the Breast Cancer Clinical Trials Program and the Inflammatory and Triple-Negative Breast Cancer Program.  Our full disclosures are available in the transcript of this episode. Dr. Shatsky, it's great to have you on the podcast today. Dr. Rebecca Shatsky: Thanks, Dr. Zibelli. It's wonderful to be here. Dr. Allison Zibelli: So, we're starting with DESTINY-Breast09, which was trastuzumab deruxtecan and pertuzumab versus our more standard regimen of taxane, trastuzumab pertuzumab for first-line treatment of metastatic HER2-positive breast cancer. Could you tell us a little bit about the study? Dr. Rebecca Shatsky: Yeah, absolutely. So, this was a long-awaited study. When T-DXd, or trastuzumab deruxtecan, really hit the market, a lot of these DESTINY-Breast trials were started around the same time. Now, this was a global, randomized, phase 3 study presented by Dr. Sara Tolaney from the Dana-Farber Cancer Institute of Harvard in Boston. It was assessing essentially T-DXd in the first-line setting for metastatic HER2-positive breast cancer in addition to pertuzumab. And that was randomized against our standard-of-care regimen, which was established over a decade ago by the CLEOPATRA trial, and we've all been using that internationally for at least the past 10 years. So, this was a large trial, and it was one-to-one-to-one of patients getting T-DXd plus pertuzumab, T-DXd alone, or THP, which mostly is used as docetaxel and trastuzumab and pertuzumab every three weeks for six cycles. And this was in over 1,000 patients; it was 1,159 patients with metastatic HER2-positive breast cancer. This was a very interesting trial. It was looking at the use of trastuzumab deruxtecan, but patients were started on this treatment for their first-line metastatic HER2-positive breast cancer with no end date to their T-DXd. So, it was, you know, you were started on T-DXd every 3 weeks until progression. Now, CLEOPATRA is a little bit different than that, though, as we know. So, CLEOPATRA has a taxane plus trastuzumab and pertuzumab. But generally, patients drop the taxane after about six to seven cycles because, as we know, you can't be really on a taxane indefinitely. You get pretty substantial neuropathy as well as cytopenias, other things that end up happening. And so, in general, that regimen has sort of a limited time course for its chemotherapy portion, and the patients maintained after the taxane is dropped on their trastuzumab and their pertuzumab, plus or minus endocrine therapy if the investigator so desires. And the primary endpoint of the trial was progression-free survival by blinded, independent central review (BICR) in the intent-to-treat population. And then it had its other endpoints as overall survival, investigator-assessed progression-free survival, objective response rates, and duration of response, and of course, safety. As far as the results of this trial, so, I think that most of us key opinion leaders in breast oncology were expecting that this was going to be a positive trial. And it surely was. I mean, this is a really, really active drug, especially in HER2-positive disease, of course. So, the DESTINY-Breast03 data really established that, that this is a very effective treatment in HER2-positive metastatic breast cancer. And this trial really, again, showed that. So, there were 383 patients that ended up on the trastuzumab plus deruxtecan plus pertuzumab arm, and 387 got THP, the CLEOPATRA regimen. What was really interesting also to note of this before I go on to the results was that 52% of patients on this trial had de novo metastatic disease. And that's pretty unusual for any kind of metastatic breast cancer trial. It kind of shows you, though, just how aggressive this disease is, that a lot of patients, they present with de novo metastatic disease. It's also reflecting the global nature of this trial where maybe the screening efforts are a little bit less than maybe in the United States, and more patients are presenting as later stage because to have a metastatic breast cancer trial in the United States with 52% de novo metastatic disease doesn't usually happen. But regardless, the disease characteristics were pretty well matched between the two groups. 54% of the patients were triple positive, or you could say hormone-positive because whether they were PR positive or ER positive and PR negative doesn't really matter in this disease. And so, the interim data cutoff was February of this year, of 2025. So, the follow-up so far has been about 29 months, so the data is still really immature, only 38% mature for progression-free survival interim analysis. But what we saw is that T-DXd plus pertuzumab, it really improved progression-free survival. It had a hazard ratio that was pretty phenomenal at 0.56 with a confidence interval that was pretty narrow of 0.44 to 0.71. So, very highly statistically significant data here. The progression-free survival was consistent across all subgroups. Overall survival, very much immature at this time, but of course, the trend is towards an overall survival benefit for the T-DXd group. The median durable response with T-DXd plus pertuzumab exceeded 3 years. Now, importantly, though, I want to stress this, is grade 3 or above treatment-emergent adverse events occurred in both subgroups pretty equally. But there were 2 deaths in the T-DXd group due to interstitial lung disease. And there was a 12.1% adjudicated drug-induced interstitial lung disease/pneumonitis event rate in the T-DXd group and only 1%, and it was grade 1-2, in the THP group. So, that's really the caveat of this therapy, is we know that a percentage of patients are going to get interstitial lung disease, and that some may have very serious adverse events from it. So, that's always something I keep in the back of my mind when I treat patients with T-DXd. And so, overall, the conclusions of the trial were pretty much a slam dunk. T-DXd plus pertuzumab, it had a highly statistically significant and clinically meaningful improvement in progression-free survival versus the CLEOPATRA regimen. And that was across all subgroups for first-line metastatic HER2-positive breast cancer here. And so, yeah, the data was pretty impressive. Just to go into the overall response rate, because that's always super important as well, you had 85.1% of patients having a confirmed overall RECIST response rate in the T-DXd plus pertuzumab group and a 78.6 in the CLEOPATRA group. The complete CR rate, complete response was 15.1% in the T-DXd group and 8.5 in the CLEOPATRA regimen. And it was really an effective regimen in this group, of course. Dr. Allison Zibelli: So, the investigators say at the end of their abstract that this is the new standard of care. Would you agree with that statement? Dr. Rebecca Shatsky: Yeah, that was a bold statement to make because I would say in the United States, not necessarily at the moment because the quality of life here, you have to think really hard about. Because one thing that's really important about the DESTINY-Breast09 data is that this was very much an international trial, and in many of the countries where patients enrolled on this, they were not able to access T-DXd off trial. And so, for them, this means T-DXd now or potentially never. And so, that is a really big difference whereas internationally, that may mean standard of care. However, in the US, patients have no issues accessing T-DXd in the second- or third-line settings. And right now, it's the standard of care in the second line in the United States, with all patients basically getting this second-line therapy except for some unique patients where they may be doing a PATINA trial regimen, which we saw at San Antonio Breast Cancer in 2024 of the triple-positive patients getting hormonal therapy plus palbociclib, which had a really great durable response. That was super impressive as well. Or there is the patient that the investigator can pick KADCYLA because the patient really wants to preserve their hair or maybe it's more indolent disease. But the quality of life on T-DXd indefinitely in the first-line setting is a big deal because, again, that CLEOPATRA regimen allows patients to drop their chemotherapy component about five to six months in. And with this, you're on a drug that feels very chemo-heavy indefinitely. And so, I think there's a lot more to investigate as far as what we're going to do with this data in the United States because it's a lot to commit a patient in the first-line metastatic setting. These de novo metastatic patients, some of them may be cured, honestly, on the HER2-targeting regimen. That's something we see these days. Dr. Allison Zibelli: So, very interesting trial. I'm sure we'll be talking about this for a long time.  So, let's move on to SERENA-6, which was, I thought, a very interesting trial. This trial took patients with ER positive, advanced breast cancer after six months on an AI (aromatase inhibitor) and a CDK4/6 inhibitor. They did ctDNA every two to three months, and when they saw an ESR1 mutation emerge, they changed half of the patients to camizestrant plus CDK4/6 and kept the other half on the AI plus CDK4/6. Can you talk about that trial a little bit, please? Dr. Rebecca Shatsky: Yeah, so this was a big trial at ASCO25. This was presented as a Plenary Session. So, this was camizestrant plus a CDK4/6 inhibitor, and it could have been any of the three, so palbo, ribo, or abemaciclib in the first-line metastatic hormone-positive population, and patients were on an AI with that. They were, interestingly, tested by ctDNA at baseline to see if they had an ESR1 mutation. So, that was an interesting feature of this trial. But patients had to have already been on their CDK4/6 inhibitor plus AI for at least 6 months to enroll. And then, as you mentioned, they got ctDNA testing every 2 to 3 months. This was also a phase 3, double-blind, international trial. And I do want to highlight again, international here, because that's important when we're considering some of this data in the U.S. because it influences some of the results. So, this was presented by Dr. Nick Turner of the Royal Marsden in the UK. So, just a little bit of background for our listeners on ESR1 mutations and why they're important. This is the most common, basically, acquired resistance mutation to patients being treated with aromatase inhibitors. We know that treatment with aromatase inhibitors can induce this. It makes a conformational change in the estrogen receptor that makes the estrogen receptor constitutively active, which allows the cell to signal despite the influence of the aromatase inhibitor to decrease the estrogen production so that the ligand binding doesn't matter as much as far as the cell signaling and transcription is concerned. And camizestrant, you know, as an oral SERD, just to explain that a little bit too; these are estrogen receptor degraders. The first-in-class of a selective estrogen receptor degrader to make it to market was fulvestrant. And that's really been our standard-of-care estrogen degrader for the past 25 years, almost 25 years. And so, a lot of us are just looking for some of these oral SERDs to replace that. But regardless, they do tend to work in the ESR1-mutated population. And we know that patients on aromatase inhibitors, the estimates of patients developing an ESR1 mutation, depending on which study you look at, somewhere between 30% to 50% overall, patients will develop this mutation with hormone-positive metastatic breast cancer. There is a small percentage of patients that have these at baseline without even treatment of an aromatase inhibitor. The estimates of that are somewhere between 0.5 and up to 5%, depending on the trial you look at and the population. But regardless, there is a chance someone on their CDK4/6 inhibitor plus AI at 6 months' time course could have had an ESR1 mutation at that time. But anyway, so they got this ctDNA every 2 to 3 months, and once they were found to develop an ESR1 mutation, the patients were then switched to the oral SERD. AstraZeneca's version of the oral SERD is camizestrant, 75 mg daily. And then their type of CDK4/6 inhibitor was maintained, so they didn't switch the brand of their CDK4/6 inhibitor, importantly. And that was looked at then for progression-free survival, but these were patients with measurable disease by RECIST version 1.1. And the data cut off here was November of 2024. This was a big trial, you know, and I think that that's influential here because this was 3,256 patients, and that's a lot of patients. So, they were all eligible. And then 315 patients ended up being randomized to switch to camizestrant upon presence of that ESR1 mutation. So, that was 157 patients. And then the other half, so they were randomized 1:1, they continued on their AI without switching to an oral SERD. That was 158 patients. They were matched pretty well. And so, their baseline characteristics, you know, the two subgroups was good. But this was highly statistically significant data. I'm not going to diminish that in any way. Your hazard ratio was 0.44. Highly statistically significant confidence intervals. And you had a median progression-free survival in those that switched to camizestrant of 16 months, and then the non-switchers was 9.2 months. So, the progression-free survival benefit there was also consistent across the subgroups. And so, you had at 12 months, the PFS rate was 60.7% for the non-treatment group and 33.4% in the treatment group. What's interesting, though, is we don't have overall survival data. This is really immature, only 12% mature as far as overall survival. And again, because this was an international trial and patients in other countries right now do not have the access to oral SERDs that the United States does, the crossover rate, they were not allowed to crossover, and so, a very few patients, when we look at progression-free survival 2 and ultimately overall survival, were able to access an oral SERD in the off-trial here and in the non-treatment group. And so, that's really important as far as we look at these results. Adverse events were pretty minimal. These are very safe drugs, camizestrant and all the other oral SERDs. They have some mild toxicities. Camizestrant is known for something weird, which is called photopsia, which is some flashing lights in the periphery of the eye, but it doesn't seem to have any serious clinical significance that we know of. It has a little bit of bradycardia, but it's otherwise really well tolerated. You know, I hate to say that because that's very subjective, right? I'm not the one taking the drug. But it doesn't have any serious adverse events that would cause discontinuation. And that's really what we saw in the trial. The discontinuation rates were really low. But overall, I mean, this was a positive trial. SERENA-6 showed that switching to camizestrant at the first sign of an ESR1 mutation on CDK4/6 inhibitor plus AI improved progression-free survival. That's all we can really say from it right now. Dr. Allison Zibelli: So, let's move on to ASCENT-04, which was a bit more straightforward. Sacituzumab govitecan plus pembrolizumab versus chemotherapy plus pembrolizumab in PD-L1-positive, triple-negative breast cancer. Could you talk about that study? Dr. Rebecca Shatsky: Yeah, so this was also presented by the lovely Sara Tolaney from Dana-Farber. And this study made me really excited. And maybe that's because I'm a triple-negative breast cancer person. I mean, not to say that I don't treat hundreds of patients with hormone- positive, but our unmet needs in triple negative are huge because this is a disease where you have got to throw your best available therapy at it as soon as you can to improve survival because survival is so poor in this disease. The average survival with metastatic triple-negative breast cancer in the United States is still 13-18 months, and that's terrible. And so, for full disclosure, I did have this trial open at my site. I was one of the site PIs. I'm not the global PI of the study, obviously. So, what this study was was for patients who had had at least a progression-free survival of 6 months after their curative intent therapy or de novo metastatic disease. They were PD-L1 positive as assessed by the Dako 22C3 assay of greater than or equal to a CPS score of 10. So, that's what the KEYNOTE-355 trial was based on as well. So, standard definition of PD-L1 positive in breast cancer here. And basically, these patients were randomized 1:1 to either their sacituzumab govitecan plus pembrolizumab, day 1 they got both therapies, and then day 8 just the saci, as is standard for sacituzumab. And then the other group got the KEYNOTE-355 regimen. So, that is pembrolizumab with – your options are carbogem there, paclitaxel or nab-paclitaxel. And it's up to investigator's decision which upon those they decided. They followed these patients for disease progression or unacceptable toxicity. It was really an impressive trial in my opinion because we know already that this didn't just improve progression-free survival, because survival is so poor in this disease, of course, we know that it improved overall survival. It's trending towards that very much, and I think that's going to be shown immediately. And then the objective response rates were better, which is key in this disease because in the first-line setting, you've got a lot of people who, especially your relapsed TNBC that don't respond to anything. And you lose a ton of patients even in the first-line setting in this disease. And so, this was 222 patients to chemotherapy and pembro and 221 to sacituzumab plus pembro. Median follow-up has only been 14 months, so it's still super early here. Hazard ratio so far of progression-free survival is 0.65, highly statistically significant, narrow confidence intervals. And so, the median duration of response here for the saci group was 16.5 months versus 9.2 months. So, you're getting a 7-month progression-free survival benefit here, which in triple negative is pretty fantastic. I mean, this reminds me of when we saw the ASCENT data originally come out for sacituzumab, and we were all just so happy that we had this tool now that doubled progression-free and overall survival and made such a difference in this really horrible disease where patients do poorly. So, OS is technically immature here, but it's really trending very heavily towards improvement in overall survival. Importantly, the treatment-related adverse events in this, I mean, we know sacituzumab causes neutropenia, people who are experienced with this drug know how to manage it at this point. There wasn't any really unexpected treatment-related adverse events. You get some people with sacituzumab who have diarrhea. It's usually pretty manageable with some Imodium. So, it was cytopenias predominantly in this disease in this population that were highlighted as far as adverse events. But I'm going to be honest, like I was surprised that this wasn't the plenary over the SERENA-6 data because this, in my mind, there we have a practice-changing trial. I will immediately be trying to use this in my PD-L1 population because, to be honest, as a triple-negative breast cancer clinical specialist, when I get a patient with metastatic triple-negative breast cancer who's PD-L1 positive, I think, "Oh, thank God," because we know that part of the disease just does better in general. But now I have something that really could give them a durable response for much longer than I ever thought possible when I started really heavily treating this disease. And so, this was immediately practice-changing for me. Dr. Allison Zibelli: I think that it's pretty clear that this is at least an option, if not the option, for this group of patients. Dr. Rebecca Shatsky: Yeah, the duration of responses here was – it's just really important because, I mean, I do think this will make people live longer. Dr. Allison Zibelli: So, moving on to the final study that we're going to discuss today, neoCARHP (LBA500), which was neoadjuvant taxane plus trastuzumab, pertuzumab, plus or minus carbo(platin) in HER2-positive early breast cancer. I think this is a study a lot of us have been waiting for. What was the design and the results of this trial? Dr. Rebecca Shatsky: I was really excited about this as well because I'm one of those people that was waiting for this. This is a Chinese trial, so that is something to take note of. It wasn't an international trial, but it was a de-escalation trial which had become really popular in HER2-positive therapy because we know that we're overtreating HER2-positive breast cancer in a lot of patients. A lot of patients we're throwing the kitchen sink at it when maybe that is not necessary, and we can really de-escalate and try to personalize therapy a little bit better because these patients tend to do well. So, the standard of care, of course, in HER2-positive curative intent breast cancer with tumors that are greater than 2 cm is to give them the TCHP regimen, which is docetaxel, carboplatin, trastuzumab, and pertuzumab. And that was sort of established by several trials in the NeoSphere trial, and now it's been repeated in a lot of different studies as well. And so, that's really the standard of care that most people in the United States use for HER2-positive curative intent breast cancer. This was a trial to de-escalate the carboplatin, which I was super excited about because many of us who treat this disease a lot think carbo is the least important part of the therapy you're giving there. We don't really know that it's necessary. We've just been doing it for a long time, and we know that it adds a significant amount of toxicity. It causes thrombocytopenia, it causes severe nausea, really bad cytopenias that can be difficult in the last few cycles of this to manage. So, this trial was created. It randomized patients one to one with stage 2 and 3 HER2-positive breast cancer to either get THP, a taxane, pertuzumab, trastuzumab, similar to the what we do in first-line metastatic HER2-positive versus the whole TCHP with a carboplatin AUC of 6, which is what's pretty standard. And it was a non-inferiority trial, so important there. It wasn't to establish superiority of this regimen, which none of us, I think, were looking for it to. And it was a modified intent-to-treat population. And so, all patients got at least one cycle of this to be assessed as a standard for an intent-to-treat trial. And so, they assumed a pCR rate of about 62.8% for both groups. And, of course, it included both HER2-positive triple positives and ER negatives, which are, you know, a bit different diseases, to be honest, but we all kind of categorize them and treat them the same. And so, this trial was powered appropriately to detect a non-inferiority difference. And so, we had about 380 patients treated on both arms, and there was an absolute difference of only 1.8% of those treated with carbo versus those without. Which was fantastic because you really realized that de-escalation here may be something we can really do. And so, the patients who got, of course, the taxane regimen had fewer adverse events. They had way fewer grade 3 and 4 adverse events than the THP group. No treatment-associated deaths occur, which is pretty standard for- this is a pretty safe regimen, but it causes a lot of hospitalizations due to diarrhea, due to cytopenias, and neutropenic fever, of course. And so, I thought that this was something that I could potentially enact, you know, and be practice-changing. It's hard to say that when it's a trial that was only done in China, so it's not necessarily the United States population always. But I think for patients moving forward, especially those with, say, a 2.5 cm tumor, you know, node negative, those, I'd feel pretty comfortable not giving them the carboplatin here. Notes that I want to make about this population is that the majority were stage 2 and not stage 3. They weren't necessarily your inflammatory HER2-positive breast cancer patients. And that the taxane that was utilized in the trial is a little different than what we use in the United States. The patients were allowed to get nab-paclitaxel, which we don't have FDA approval for in the first-line curative intent setting for HER2-positive breast cancer in the United States. So, a lot of them got abraxane, and then they also got paclitaxel. We tend to use docetaxel every 3 weeks in the United States. So, just to point out that difference. We don't really know if that's important or not, but it's just a little bit different to the population we standardly treat. Dr. Allison Zibelli: So, are there patients that you would still give TCHP to? Dr. Rebecca Shatsky: Yeah, great question. I've been asked that a lot in the past like week since ASCO. I'd say in my inflammatory breast cancer patients, that's a group I do tend to sometimes throw the kitchen sink at. Now, I don't actually use AC in those because I know that that was the concern, but I think the TRAIN-2 trial really showed us you don't need to use Adriamycin in HER2-positive disease unless it's like refractory. So, I don't know that I would throw this on my stage 3C or inflammatory breast cancer patients yet because the majority of this were not stage 3. So, in your really highly lymph node positive patients, I'm a little bit hesitant to de-escalate them from the start. This is more of a like, if there's serious toxicity concerns, dropping carbo is absolutely fine here. Dr. Allison Zibelli: All right, great.  Thank you, Dr. Shatsky, for sharing your valuable insights with us on the ASCO Daily News Podcast today. Dr. Rebecca Shatsky: Thanks so much, Dr. Zibelli and ASCO Daily News. I really want to thank you for inviting me to talk about this today. It was really fun, and I hope you find my opinions on some of this valuable. And so, I just want to thank everybody and my listeners as well. Dr. Allison Zibelli: And thank you to our listeners for joining us today. You'll find the links to all the abstracts discussed today in the transcript of this episode. Finally, if you like this podcast and you learn things from it, please take a moment to rate, review, and describe because it helps other people find us wherever you get your podcasts. Thank you again. 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. More on today's speakers Dr. Allison Zibelli Dr. Rebecca Shatsky @Dr_RShatsky Follow ASCO on social media:  @ASCO on Twitter  @ASCO on Bluesky  ASCO on Facebook  ASCO on LinkedIn   Disclosures: Dr. Allison Zibelli: No relationships to disclose Dr. Rebecca Shatsky: Consulting or Advisory Role: Stemline, Astra Zeneca, Endeavor BioMedicines, Lilly, Novartis, TEMPUS, Guardant Health, Daiichi Sankyo/Astra Zeneca, Pfizer Research Funding (Inst.): OBI Pharma, Astra Zeneca, Greenwich LifeSciences, Briacell, Gilead, OnKure, QuantumLeap Health, Stemline Therapeutics, Regor Therapeutics, Greenwich LifeSciences, Alterome Therapeutics