Podcasts about dana farber cancer institute

As part of the European Society for Medical Oncology (ESMO) Congress 2025, CancerNetwork® spoke with a variety of experts about key takeaways from different late-breaking abstracts, oral presentations, and other sessions focused on potential advancements across cancer care. Presenting investigators highlighted updated results from clinical trials evaluating novel therapeutic strategies across different cancer populations, including breast cancer and lung cancer.  Phase 3 VIKTORIA-1 Trial Sara A. Hurvitz, MD, FACP, the Smith Family Endowed Chair in Women's Health and senior vice president and director of the Clinical Research Division at the Fred Hutch Cancer Center, and tumor chair in breast oncology for the ONCOLOGY® editorial advisory board, first discussed findings from the phase 3 VIKTORIA-1 trial (NCT05501886). Her presentation highlighted how VIKTORIA-1 was “the first study to demonstrate a statistically significant and clinically meaningful improvement in progression-free survival [PFS] with PAM inhibition” for patients with PIK3CA wild-type advanced breast cancer. Data from the trial showed that gedatolisib plus fulvestrant (Faslodex) and palbociclib (Ibrance) produced a median PFS of 9.3 months (95% CI, 7.2-16.6) vs 2.0 months (95% CI, 1.8-2.3) with fulvestrant alone (HR, 0.24; 95% CI, 0.17-0.35; P

In this episode of the Oncology Brothers podcast, we dive into the groundbreaking data presented at ESMO 2025, focusing on the GU landscape, particularly prostate and bladder cancer. Join us as we welcome Dr. Stephanie Berg, a GU medical oncologist from the Dana-Farber Cancer Institute, to discuss key studies and their implications for patient care. Episode Highlights: ⁠PSMAddition: Explore the benefits of lutetium PSMA in metastatic hormone-sensitive prostate cancer, including improved radiographic progression-free survival when combined with ADT and ARPIs. Capitello-281: Highlights the use of Capivasertib in patients with PTEN loss, showing significant improvements in radiographic PFS. Potomac: Examining the role of durvalumab + BCG in high-risk non-muscle invasive bladder cancer, and the promising results from the Keynote 905 study involving enfortumab and pembrolizumab. IMVigor011: Delved into showcasing how ctDNA-guided therapy with atezolizumab can improve survival outcomes. Stay tuned as we navigate the complexities of treatment options, side effects, and the importance of patient-centered decision-making in oncology.  Follow us on social media: •⁠  ⁠X/Twitter: https://twitter.com/oncbrothers •⁠  ⁠Instagram: https://www.instagram.com/oncbrothers •⁠  Website: https://oncbrothers.com/ Don't forget to subscribe for more insights on treatment algorithms, FDA approvals, and conference highlights! #ESMO2025 #GUOncology #LutetiumPSMA #Enfortumab #BladderCancer #ProstateCancer #OncologyBrothers

In this episode of The HemOnc Pulse, host Melissa speaks with Omar Nadeem, MD, Senior Physician at Dana-Farber Cancer Institute and Assistant Professor of Medicine at Harvard Medical School, about emerging genomic insights in smoldering multiple myeloma. The discussion focuses on recent research showing how molecular profiling can improve understanding of disease progression and refine risk stratification beyond traditional clinical models. Dr. Nadeem highlights how genomic data may help distinguish patients with smoldering myeloma who are at higher risk of progression from those likely to remain stable, offering the potential to guide more personalized treatment decisions. The conversation also explores the evolving landscape of precursor plasma cell disorders and the role of immunotherapy, including CAR T-cell therapy, in clinical management.      

Host: Charles Turck, PharmD, BCPS, BCCCP Guest: Sarah Sammons, MD About 40 percent of patients with metastatic HR+/HER2- breast cancer have an activating mutation in the PIK3CA gene,1,2 which plays a key role not only in tumor growth, but also in driving resistance to endocrine therapy.3-5 And while there are several FDA-approved PI3K pathway-targeted agents for patients with PIK3CA tumor mutations,6-8 they come with challenges, like modest efficacy and on-pathway effects.9-12 Given this unmet need, the ReDiscover trial evaluated the investigational agent RLY-2608 in combination with fulvestrant in in patients with PIK3CA-mutated HR+/HER2- aBC previously treated with a CDK4/6 inhibitor.13 Joining Dr. Charles Turck to share updated safety and efficacy data from the trial is Dr. Sarah Sammons, a Senior Physician at the Dana-Farber Cancer Institute and an Assistant Professor of Medicine at Harvard Medical School in Boston. References: Vasan N, Cantley LC, Vasan N, Cantley LC. At a crossroads: how to translate the roles of PI3K in oncogenic and metabolic signalling into improvements in cancer therapy. Nat Rev Clin Oncol. 2022;19(7):471-485. doi:10.1038/s41571-022-00633-1 Network TCGA. Comprehensive molecular portraits of human breast tumours. Nature. 2012;490(7418):61-70. doi:10.1038/nature11412 Saal LH, Johansson P, Holm K, et al. Poor prognosis in carcinoma is associated with a gene expression signature of aberrant PTEN tumor suppressor …

Eric Fischer, a professor at Dana-Farber Cancer Institute, on creating a new class medicines -- targeted protein degraders.

JCO PO author Dr. Asaf Maoz at Dana-Farber Cancer Institute shares insights into article, “Causes of Death Among Individuals with Lynch Syndrome in the Immunotherapy Era.” Host Dr. Rafeh Naqash and Dr. Maoz discuss the causes of death in individuals with LS and the evolving role of immunotherapy. TRANSCRIPT Dr. Rafeh Naqash: Hello, and welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCOPO articles. I'm your host, Dr. Rafeh Naqash, podcast editor for JCO Precision Oncology and Associate Professor Medicine, at the OU Health Stephenson Cancer Center. Today, I'm super thrilled to be joined by Dr. Asaf Maoz, Medical Oncologist at Dana-Farber Cancer Institute, Brigham and Women's Hospital, and faculty at the Harvard Medical School, and also lead author on the JCO Precision Oncology article entitled "Causes of Death Among Individuals with Lynch Syndrome in the Immunotherapy Era." This publication will be a concurrent publication with an oral presentation at the annual CGA meeting. At the time of this recording, our guest's disclosures will be linked in the transcript. Asaf, I'm excited to welcome you on this podcast. Thank you for joining us today. Dr. Asaf Maoz: Thank you so much for highlighting our paper. Dr. Rafeh Naqash: Absolutely. And I was just talking to you that we met several years back when you were a trainee, and it looks like you've worked a lot in this field now, and it's very exciting to see that you consider JCOPO as a relevant home for some of your work. And the topic that you have published on is of significant interest to trainees from a precision medicine standpoint, to oncologists in general, covers a lot of aspects of immunotherapy. So, I'm really excited to talk to you about all of this. Dr. Asaf Maoz: Me too, me too. And yeah, I think JCOPO has great content in the area of cancer genetics and has done a lot to disseminate the knowledge in that area. Dr. Rafeh Naqash: Wonderful. So, let's get started and start off, given that we have hosts of different kinds of individuals who listen to this podcast, especially when driving from home to work or back, for the sake of making everything simple, can we start by asking you what is Lynch syndrome? How is it diagnosed? What are some of the main things to consider when you're trying to talk an individual where you suspect Lynch syndrome? Dr. Asaf Maoz: Lynch syndrome is an inherited predisposition to cancer, and it is common. So, we used to think that, or there's a general notion in the medical community that it is a rare condition, but we actually know now from multiple studies, including studies that look at the general population and do genetic testing regardless of any clinical phenotype, that Lynch syndrome is found in about 1 in 300 people in the general population. If you think about it in the United States, that means that there are over a million people living with Lynch syndrome in the United States. Unfortunately, most individuals with Lynch syndrome don't know they have Lynch syndrome at the current time, and that's where a lot of the efforts in the community are being made to help detect more individuals who have Lynch syndrome. Lynch syndrome is caused by pathogenic germline variants in mismatch repair genes, MLH1, MSH2, MSH6, or PMS2, or as a result of pathogenic variants in EPCAM that cause silencing of the MSH2 gene. Dr. Rafeh Naqash: Excellent. Thank you for that explanation. Now, one of the other things I also realized, similar to BRCA germline mutations, where you require a second hit for individuals with Lynch syndrome to have mismatch repair deficient cancers, you also require a second hit to have that second hit result in an MSI-high cancer. Could you help us understand the difference of these two concepts where generally Lynch syndrome is thought of to be cancers that are mismatch repair deficient, but that's not necessarily true for all cases as we see in your paper. Can you tease this out for us a little bit more? Dr. Asaf Maoz: Of course, of course. So, the germline defect is in one of the mismatch repair genes, and these genes are responsible for DNA mismatch repair, as their name implies. Now, in a normal cell, we think that one working copy is generally enough to maintain the mismatch repair machinery intact. What happens in tumors, as you alluded to, is that there is a second hit in the same mismatch repair gene that has the pathogenic germline variant, and that causes the mismatch repair machinery not to work anymore. And so what happens is that there is formation of mutations in the cancer cell that are not present in other cells in the body. And we know that there are specific types of mutations that are associated with defects in mismatch repair mechanisms, and those are associated a lot of times with frameshift mutations. And we have termed them ‘microsatellites'. So there are areas in the genome that have repeats, for example, you know, if you have AAAA or GAGA, and those areas are particularly susceptible to mutations when the mismatch repair machinery is not working. And so we can measure that with DNA microsatellite instability testing. But we can also get a sense of whether the mismatch repair machinery is functioning by looking at protein expression on the surface of cancer cells and by doing immunohistochemistry. More recently, we're also able to infer whether the mismatch repair machinery is working by doing next-generation sequencing and looking at many, many microsatellites and whether they have this DNA instability in the microsatellites. Dr. Rafeh Naqash: Excellent explanation. As a segue to what you just mentioned, and this reminds me of some work that one of my good friends, collaborators, Amin Nassar, whom you also know, I believe, had done a year and a half back, was published in Cancer Cell as a brief report, I believe, where the concept was that when you look at these mismatch repair deficient cancers, there is a difference between NGS testing, IHC testing, and maybe to some extent, PCR testing, where you can have discordances. Have you seen that in your clinical experience? What are some of your thoughts there? And if a trainee were to ask, what would be the gold standard to test individuals where you suspect mismatch repair deficient-related Lynch syndrome cancers? How would you test those individuals? Dr. Asaf Maoz: We do sometimes see discordance, you know, from large series, the concordance rate is very high, and in most series it's over 95%. And so from a practical perspective, if we're thinking about the recommendation to screen all colorectal cancer and all endometrial cancer for mismatch repair deficiency, I think either PCR-based testing or immunohistochemistry is acceptable because the concordance rate is very high. There are rare cases where it is not concordant, doing multiple of the tests makes sense at that time. If you think about the difference between the tests, the immunohistochemistry looks at protein expression, which is a surrogate for whether there is mismatch repair deficiency or not, right? Because ultimately, the mismatch repair deficiency is manifested in the mutations. So if the PCR does not show microsatellite instability and now NGS does not show microsatellite instability, the IHC may be a false positive. At the end of the day, the functional analysis of whether there are actually unstable microsatellites either by PCR or by NGS is what I would consider more informative. But IHC again is an excellent test and concordant with those results in over 95% of cases. Now there is also an issue of sampling. It's possible that there's heterogeneity within the tumor. We published a case in JCOPO about heterogeneity of the mismatch repair status, and that was both by immunohistochemistry, but also by PCR. So there are some caveats and interpreting these tests does require some expertise, and I'm always happy to chat with trainees or whoever has an interesting or challenging case. Dr. Rafeh Naqash: Thanks again for that very easy to understand explanation. Now going to management strategies, could you elaborate a little bit upon the neo-adjuvant data currently, or the metastatic data which I think more people are familiar with for immunotherapy in individuals with MSI-high cancers? Dr. Asaf Maoz: Yeah, that's an excellent question and obviously a very broad topic. Individuals with Lynch syndrome typically develop tumors that are mismatch repair deficient or microsatellite unstable. And we have seen over the last 15 years or so that these tumors, because they have a lot of mutations and because these mutations are very immunogenic, we have seen that they respond very well to immunotherapy. And this has been shown across disease sites and has been shown across disease settings. And for that reason, immunotherapy was approved for MSI-high or mismatch repair deficient cancer regardless of the anatomic site. It was the first tissue-agnostic approval by the FDA in 2017. And so there are exciting studies both in the metastatic setting where we see individuals who respond to immunotherapy for many years, and one could wonder whether their cancer is going to come back or not. And also in the earlier setting, for example, the Cercek et al. study in the New England Journal from Sloan Kettering, where they showed that neoadjuvant immunotherapy can cause durable responses for rectal cancer that is mismatch repair deficient. And in that series, the patients did not require surgery or radiation, which is standard of care for rectal cancer otherwise. And there's also exciting data in the adjuvant space, as was presented in ASCO by Dr. Sinicrope, the ATOMIC study, and many more efforts to bring immunotherapy into the treatment landscape for individuals with MSI-high cancer, including individuals with Lynch syndrome. Dr. Rafeh Naqash: A lot of activity, especially in the neo-adjuvant and adjuvant space over the last two years or so. Now going to the actual reason why we are here is your study. Could you tell us why you looked at this idea of patients who had Lynch syndrome and died, and the reasons for their death? What was the thought that triggered this project? Dr. Asaf Maoz: As we were talking about, we now know that immunotherapy really has changed the treatment landscape for individuals with Lynch syndrome, and that most cancers that individuals with Lynch syndrome do have this mismatch repair deficiency. But we also know that individuals with Lynch syndrome can develop tumors that do not have mismatch repair deficiency, and we call them mismatch repair proficient or microsatellite stable. And there was a series from Memorial Sloan Kettering showing that in colorectal cancer, about 10% of the tumors that individuals with Lynch syndrome developed did not have mismatch repair deficiency. In addition to that, we anecdotally saw that some of our patients with Lynch syndrome died of causes that were not mismatch repair deficient tumors. We wanted to see how that has changed since immunotherapy was approved in a tissue-agnostic manner, meaning that we could look at this regardless of where the cancer started, because we would anticipate that if the tumor was mismatch repair deficient, the patient would be able to access immunotherapy as standard of care. Dr. Rafeh Naqash: Thank you. And then you looked at different aspects of correlations with regards to individuals that had an MSI-high cancer with Lynch syndrome or an MSS cancer with Lynch syndrome. Could you elaborate on some of the important findings that you identified as well as some of the unusual findings that perhaps we did not know about, even though the sample size is limited, but what were some of the unique things that you did identify through this project? Dr. Asaf Maoz: The first question was what cause is leading to death in individuals with Lynch syndrome? And we had 54 patients that we identified that had died since the approval of immunotherapy in 2017, 44 of which died of cancer-related causes. And when we looked at cancer-related causes of death, we wanted to know how many of those were due to mismatch repair deficient tumors versus mismatch repair proficient tumors or MS-stable tumors. And we found, somewhat surprisingly, that 43% of patients in our cohort actually died of tumors that were microsatellite stable or mismatch repair proficient, meaning of tumors that are not typically associated with Lynch syndrome. This is not entirely surprising as a cause of death because we know that immunotherapy does not typically work for tumors that are microsatellite stable. And so in the metastatic setting, there are much less cases of durable remissions with treatment. But it was helpful to have that figure as an important benchmark. There are previous studies about causes of death in Lynch syndrome, and particularly from the Prospective Lynch Syndrome Database in Europe. Those have provided really important information about cause of death by cancer site, but they typically don't have mismatch repair status and are more difficult to interpret in that regard. They also don't include a large number of individuals who have PMS2 Lynch syndrome, which is the most common, but least penetrant form of Lynch syndrome. Dr. Rafeh Naqash: As far as the subtype of pathogenic germline variants is concerned, did you notice anything unusual? And I've always had this question, and you may know more about this data, is: In the bigger context of immunotherapy, does the type of the pathogenic germline variant for Lynch syndrome associated MSI-high cancers, does that impact or have an association with the kind of outcomes, how soon a cancer progresses or how many exceptional responders perhaps with MSI-high cancers actually have a certain specific pathogenic germline variant? Dr. Asaf Maoz: That's an excellent question, and certainly we need more data in that space. We know that the type of germline mutation, or the gene in which there is a germline pathogenic variant, determines to a large degree the cancer risk, right? So we know that individuals who have germline pathogenic variants in MLH1 or MSH2 have a much higher colorectal cancer risk than, for example, PMS2. We know that for PMS2, the risks are more limited to colorectal and endometrial, and may be lower risk of other cancers. We also know that, you know, the spectrum of disease may change based on the pathogenic germline variants. For example, individuals who have MSH2 associated Lynch syndrome have more risk of additional cancers in other organs like the urinary tract and other less common Lynch-associated tumors. The question about response to therapy is one where we have much less information. There are studies that are trying to assess this, but I don't think the answer is there yet. Some of the non-clinical data looks at how many mutations there are based on the pathogenic variant and what the nature of those mutations are, whether they're more frameshift or others. But I think we still need more clinical data to understand whether the response to immunotherapy differs. It's also complicated by the fact that the immunotherapy landscape is changing, especially in the metastatic setting, now with the approval of combination ipilimumab and nivolumab for first-line treatment of colorectal cancer that is microsatellite unstable. But in our study, we did find that, as you would expect, there is an enrichment in MS-stable cancers among those with PMS2 Lynch syndrome. Again, our denominator is those who died, right? So this is not the best way to look at the question whether this is overall true, that is more addressed by the study that Sloan Kettering published. But we do see, as we would anticipate, that there are more microsatellite stable cancers among those with PMS2 Lynch syndrome that died. Dr. Rafeh Naqash: A lot to uncover there for sure. This study and perhaps some of the other work that you're doing is slowly advancing our understanding of some of these concepts. So I'd like to shift gears to a couple of provocative questions that I generally like to ask. The first is, in your opinion, and you may or may not have data to back this up, which is okay, and that's why we're having a conversation about it. In your opinion, do you think the type or the quality of the neoantigen is different based on the pathogenic germline variant and a Lynch syndrome associated MSI-high cancer? Dr. Asaf Maoz: I think there are some data out there that, you know, I can't cite off the top of my mind, but there are some data out there that suggest that that may be the case. I think the key question is the quality, right? I think that whether these differences that are found on a molecular level also translate to a clinical difference in response is something that is unknown at this moment. Some people hypothesize that if the tumor has less neoantigens, there's less of a response to immunotherapy. But I think we really need to be careful before making those assertions on a clinical level. I do think it's a really important question that needs to be answered, among others because, you know, in the colorectal space, for example, where we have both the option of doing ipilimumab with nivolumab and the option of doing pembrolizumab, we don't really know which patients need the CTLA-4 blockade versus which patients can receive PD-1 blockade alone and avoid the potential excess toxicity of the CTLA-4 blockade. There are a lot of interesting questions there that still need to be answered. And of course, individuals with Lynch syndrome are just a fraction of those individuals who have MSI-high cancer. So there's also the question about whether non-Lynch syndrome associated MSI-high cancer responds differently to immunotherapy than Lynch syndrome associated MSI-high cancer. A lot of very interesting questions in the field for sure. Dr. Rafeh Naqash: Absolutely. My second question is more about trying to understand the role of ctDNA, MRD monitoring in individuals with Lynch syndrome. If somebody has a germline, you know, Lynch syndrome MSI-high cancer, when you do a tumor-informed ctDNA assessment, what do you capture generally there? Because, and this question stems from a discussion I've had with somebody regarding EGFR lung cancer, since I treat individuals with lung cancer, and the concept generally is that even if the tissue showed EGFR, but for MRD monitoring, when you do a barcoded sequence of different tumor specific mutations, it's not actually the EGFR that they track in the blood when they do ctDNA assessment. But from a Lynch syndrome standpoint, if you have a germline, right, which is the first hit, and then you have the somatic in the tumor, which is the second hit, are you aware or have you tried to look into this where what is exactly being followed if one had to follow MRD in a Lynch syndrome MSI-high colorectal cancer? Dr. Asaf Maoz: I think a lot of the MRD assays are proprietary, and so we don't receive information about what the mutations that are being tracked are. In general, the idea is to track mutations that we would not expect to disappear as part of resistant mechanisms. We want these to be truncal mutations. We want these to be mutations in which resistance is not expected to result in reversion mutations. But what specifically is being tracked is something that I don't know because these assays, the tumor-informed ones, are proprietary, and we don't get the results regarding specific mutations. When it's circulating tumor DNA that is not necessarily tumor-informed, we do get those results, but that is less so about the specific selection of mutations. Dr. Rafeh Naqash: Thank you for clarifying that question to some extent, of course, as you said, we don't know a lot, and we don't know what we don't know. That's the most important thing that I've learned in the process of understanding precision medicine and genomics, and it's a very fast-paced evolving field. Last question related to your project, what is the next step? Are you planning any next steps as a bigger multicenter study or validation of some sort? Dr. Asaf Maoz: There are two big questions that this study raises. One, is this true across multiple other sites, right? Because this is a single center study, and we really need additional centers to look at their data and validate whether they are also seeing that a substantial portion of deaths in individuals with Lynch syndrome are attributable to mismatch repair proficient cancer. The other question is whether we can look at specifically MSI-high cancer versus MS-stable cancer and understand what the mortality rate for each of those are. From a clinical perspective, it's important to counsel individuals with Lynch syndrome about general cancer screening outside of mismatch repair deficient tumors and to understand that there is also a risk of mismatch repair proficient tumors and that treatment for those tumors would be different. There's a lot of work to be done in the future. Another major area of need is to see whether tumors that are microsatellite stable can be sensitized to immunotherapy, and that is beyond the Lynch syndrome field, but that is something that certainly would benefit these individuals with Lynch syndrome who develop mismatch repair proficient cancer. Dr. Rafeh Naqash: That's very interesting to hear, and we'll look forward to seeing some of those developments shape in the next few years. Now, I'd like to spend a minute, minute and a half on you specifically as a researcher, clinician, scientist. Could you briefly highlight - because I remember meeting you several years back as a trainee, with your interest in genomics, computational research - could you briefly tell us what led you to hereditary cancer syndromes based on your research and work? What are some of the things that you learned along the way that other early career investigators can perhaps take lessons from? Dr. Asaf Maoz: Big questions there, thanks for asking. I got interested in the field of hereditary cancer syndromes when I came to the United States and started doing lab research in Stephen Gruber's lab at the time at USC. He's now at City of Hope. And my interest was originally looking at immunotherapy and immunology, but I went to the case conferences where we were learning about individuals with hereditary cancer, and those were kind of earlier days where we were still trying to figure out how to test and what the implications for these individuals would be. And through fellowship, I was also very interested in that, and I did my senior fellowship years with Dr. Yurgelun here at Dana-Farber, who is the director of the Lynch Syndrome Center. And I I think it's the combination between being able to treat individuals based on precision medicine and what the germline mutation is, but also the ability to prevent cancer and to develop strategies to intercept cancer early that is really appealing to me in this field. It's also a great field to be in because it's a small field. If you come to the CGA-IGC meeting, you'll be able to interact with everyone. Everyone is super collaborative, super nice, and I really recommend it to trainees. The CGA-IGC annual meeting is really a great opportunity to learn more and experience some of the advancement specifically in the GI hereditary space. Lessons for trainees. I think there are a lot of lessons that I could think about, but I think finding strong and supportive mentors is one of the things that has helped me most. I think that just having close relationship with your mentor, having frequent discussions and honest discussions about what is feasible, what is going to make a difference for your patients and your research and what you want to focus on is really important. And so I think if I had to choose one thing, I would say choose a mentor that you trust, that you feel you have a good relationship with, and that has the availability to support you. Dr. Rafeh Naqash: Thank you so much for those insightful comments, and thank you for sharing with us your journey, your project, and some of your interesting thoughts on this concept of hereditary cancers. Hopefully, we'll see more of this work being published in JCOPO through your lab or work from others. Dr. Asaf Maoz: Thank you so much. I appreciate the opportunity to be here. Dr. Rafeh Naqash: Thank you for listening to JCO Precision Oncology Conversations. Don't forget to give us a rating or review and be sure to subscribe so you never miss an episode. You can find all ASCO shows at 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.

Cancer used to be something you worried about later in life — but not anymore. More and more young adults are being diagnosed, and doctors are trying to figure out why this is happening. Dr. Sanjay Gupta talks with oncologist Dr. Kimmie Ng about what's behind this rise, why colorectal cancer is leading the trend, and the signs you shouldn't ignore.  You can find more information and resources at the Young-Onset Colorectal Cancer Center at the Dana-Farber Cancer Institute.    This episode was produced by Kyra Dahring.    Medical Writer: Andrea Kane Showrunner: Amanda Sealy Senior Producer: Dan Bloom Technical Director: Dan Dzula  Learn more about your ad choices. Visit podcastchoices.com/adchoices

Dr Jeremy S Abramson from Massachusetts General Hospital in Boston, Dr Jennifer Crombie from Dana-Farber Cancer Institute also in Boston and Dr Laurie H Sehn from the BC Cancer Centre for Lymphoid Cancer in Vancouver, British Columbia, Canada, discuss recent updates on available and novel treatment strategies for follicular lymphoma.  CE information and select publications here.

On this episode of SurgOnc today, Dr. Rosalinda Alvarado and Dr. George Molina moderate a discussion on how to improve the recruitment of Hispanic/Latino patients into clinical trials. Joining the conversation are Jeanette Gonzalez from the University of Illinois Cancer Center and Alas-Wings, Dr. Narjust Florez from Dana-Farber Cancer Institute and Harvard Medical School, and Dr. Kennedy Timothy from MedStar Health and Georgetown University.

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Scott A. Armstrong, M.D., Ph.D., of the Dana-Farber Cancer Institute, studies how certain aggressive forms of acute myeloid leukemia (AML) develop and survive. His work centers on a protein called menin, which helps leukemia cells keep cancer-promoting genes switched on. Armstrong's team has found that blocking menin with specially designed drugs can shut down these gene programs, push leukemia cells to mature, and slow or stop the disease in lab models and patients. While some leukemias adapt by developing mutations in menin or finding other ways to survive, his research is revealing why certain genes are especially dependent on menin and how to target them more effectively. These discoveries are now shaping new treatments, drug combinations, and potential strategies for other cancers that rely on similar mechanisms. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40875]

Here in the West, acupuncture often feels like something foreign, something patients approach with curiosity but no context. “I don't know anything about Chinese medicine,” they'll say. And most of the time, that's true. We didn't grow up with an uncle who prescribed herbs or a parent using needles to ease the illnesses and injuries of childhood.For Wei Dong Lu, medicine wasn't foreign at all. He grew up inside it, part of a family where healing was daily life. At sixteen, during the Cultural Revolution, he was told to learn a “practical skill.” His classmates were sent to carpentry or sewing. He was handed needles. Listen into this discussion as we trace the path that took him from Shanghai to Nebraska, from teaching at the New England School of Acupuncture to practicing oncology acupuncture at Harvard's Dana-Farber Cancer Institute.What you'll hear isn't just the biography of one practitioner, but a story about how medicine travels—how it bends and blends to circumstance, how it adapts to new settings, and how something essential continues to move through it all.

If more and more young people are dying of colorectal cancer, why aren't we talking about it? Is it because we're too ashamed of our bodies?Rates of colorectal cancer are rising, especially for people under 50. But it's hard to raise awareness for a cancer that a lot of us find hard to talk about. In a recent essay for The Cut, writer Laurie Abraham described her experience of colon cancer, which included a lot of embarrassment. Talking about your bowel movements is...not fun. Can you relate?Today, Brittany is joined by Laurie and Dr. Kimmie Ng, Co-Director of the Colon and Rectal Cancer Center at the Dana-Farber Cancer Institute, to get into the cultural shame around how we talk about colon cancer - and how that extends to a lack of funding and research.Follow Brittany Luse on Instagram: @bmluseFor handpicked podcast recommendations every week, subscribe to NPR's Pod Club newsletter at npr.org/podclub.Learn more about sponsor message choices: podcastchoices.com/adchoicesNPR Privacy Policy

In this episode, Sara Tolaney, MD, of Dana-Farber Cancer Institute, discusses sequencing strategies after progression in...

In this episode, Sara Tolaney, MD, of Dana-Farber Cancer Institute, discusses sequencing strategies after progression in HER2-positive metastatic breast cancer. She reviews current second-line standards, considerations for patients with brain metastases, and emerging therapies in the post–T-DXd setting.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. Lachelle Weeks is a physician-scientist at Dana-Farber Cancer Institute working on a project to predict leukemia risk based on widely available blood samples.

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

Shoot us a Text.On this Saturday, Chris joins Paul and Kyle to talk about the power of remembrance and how Carla Cosenzi and TommyCar Auto Group are connecting people in a meaninful way through the 17th Annual Tom Cosenzi Driving for the Cure Charity Golf Tournament.Founded in memory of Tom Cosenzi, the event supports Dana-Farber Cancer Institute and the incredible work of Dr. Wen and his team.Golfers, sponsors, and volunteers showed up in full force to continue the mission of giving back.Carla Cosenzi on LinkedIn said “Dad, I hope you are proud of what has been built in your name… Together, we are making a difference.”Join Paul J Daly and Kyle Mountsier every morning for the Automotive State of the Union podcast as they connect the dots across car dealerships, retail trends, emerging tech like AI, and cultural shifts—bringing clarity, speed, and people-first insight to automotive leaders navigating a rapidly changing industry.Get the Daily Push Back email at https://www.asotu.com/ JOIN the conversation on LinkedIn at: https://www.linkedin.com/company/asotu/

In today's episode, supported by Chimerix, we spoke with Patrick Y. Wen, MD, about the FDA approval of dordaviprone (Modeyso) for the treatment of adult and pediatric patients at least 1 year of age with H3K27M-mutated diffuse midline glioma who have progressive disease following prior therapy. Dr Wen is the director of the Center for Neuro-Oncology at Dana-Farber Cancer Institute; as well as a professor of neurology at Harvard Medical School in Boston, Massachusetts. In our conversation, Dr Wen discussed the significance of this accelerated approval across patient age groups, key efficacy and safety data that supported this approval, and the importance of biomarker testing in patients with glioma. He also highlighted potential next steps for expanding the investigation of dordaviprone in patients with glioma and emphasized the ways that multidisciplinary collaboration can provide patients with personalized, optimized care. 

Small cell lung cancer was once considered one of the most challenging diagnoses in oncology. But today, groundbreaking treatments are transforming patient outcomes and rewriting survival stories. Discover how immunotherapy, T-cell engagers, CAR T-cell therapy, and antibody drug conjugates are moving from clinical trials to standard care, offering patients years of disease control and genuine hope for the future. Featuring insights from Dr. Jacob Sands, thoracic oncologist at Dana-Farber Cancer Institute, and inspiring patient advocate Wendy Brooks, who shares her powerful journey from early detection through cutting-edge clinical trials, proving that advocacy and hope can change everything. Guests: Dr. Jacob Sands, Oncologist, Dana-Farber Cancer Institute Courtney Mantz, Program Manager II, SCLC Program, Dr. Sands' Assistant. Dana-Farber Cancer Institute, Lowe Center for Thoracic Oncology Wendy Brooks, Patient Advocate Show Notes | Transcript | Watch Video

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. 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?

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.

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.

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.

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.

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

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.

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

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.

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.

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.

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

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

“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