Podcasts about mskcc

In this episode, we explore the emerging entity of CAR Transgenic T-cell Lymphoproliferative Neoplasms (CTTLN), a rare but important complication of CAR T-cell therapy. Dr. Piers Blombery from Peter MacCallum Cancer Center joins us to dissect two cases from the CARTITUDE-4 trial where patients developed T-cell lymphomas expressing the chimeric antigen receptor following cilta-cel treatment for multiple myeloma. As a bonus, we also briefly discussed Dr. Blombery's paper on menin inhibitors in UBTF tandem duplicated AML. Here are the papers we discussed: 1. CTTLN cases from CARTITUDE-4: https://pubmed.ncbi.nlm.nih.gov/39938094/2. CTTLN case from MSKCC with insertional mutagenesis: https://pubmed.ncbi.nlm.nih.gov/39908432/3. Other CTTLN cases in myeloma: https://pubmed.ncbi.nlm.nih.gov/38865661/https://pmc.ncbi.nlm.nih.gov/articles/PMC8417502/4. Response and resistance to menin inhibitors in UBTF tandem duplication AML: https://pubmed.ncbi.nlm.nih.gov/38924737/

Gopa Iyer from MSKCC joins the show to discuss his initial results from this phase 2 trial.

In this episode, we sit down with Sarah Bugen, a nurse at Memorial Sloan Kettering Cancer Center, who shares her expertise on managing life after a blood or bone marrow transplant, particularly in relation to chronic graft-versus-host disease (GVHD). The conversation centers on practical advice for patients and caregivers navigating recovery and maintaining quality of life.Regarding Oral GVHD, Sarah emphasizes the importance of oral health post-transplant, recommending soft toothbrushes, alcohol-free mouthwash, and avoiding irritants like spicy or acidic foods. She suggests soft, hydrating foods and stresses the need for regular dental checkups with oncologist approval. Hydration is vital for managing dry mouth, with a goal of 2-3 liters of fluids daily. Also, sugarless candy or gum can help stimulate saliva production.For nutrition, Sarah advises increasing caloric intake with protein powders, full-fat products, and small, frequent meals. She also highlights the value of bland diets and electrolyte packets for hydration. Avoiding triggers like dairy, caffeine, and greasy foods can minimize gastrointestinal discomfort (and even GVHD of the GI Tract), while clean cooking practices ensure safety during recovery.Skin care is another focus. Sarah recommends fragrance-free, gentle products like CeraVe and Cetaphil and suggests applying moisturizer after a shower to lock in hydration. Sunscreen, protective clothing, and sun hats are essential, even in winter, to protect sensitive post-transplant skin.Physical activity is vital for rebuilding strength and improving mental health. Sarah advises patients to start slow with light activities like walking or stretching and gradually increase as tolerated. Physical therapy exercises should be integrated into daily routines, and adequate rest is crucial after any activity.  Even though it may be counter-intuitive, continuous movement is key in the battle against fatigue.Caregivers also play a pivotal role. Sarah underscores the importance of open communication with the medical team and notes that caregivers can support medication management, track progress, and join support groups for additional resources. Caregivers are encouraged to celebrate small victories and take care of their own mental health, as they are an essential part of the recovery process.Finally, Sarah shares an incredible survivor story, and reflects on the resilience in her patients and the importance of celebrating milestones like “transplant birthdays.” She encourages patients to set realistic goals, maintain hope, and focus on incremental progress. Sarah leaves us with an inspiring reminder to be patient with ourselves, celebrate every achievement, and never stop fighting.Resources:Link to LLS free Nutrition Consultations: https://www.lls.org/managing-your-cancer/food-and-nutritionGVHD Alliance: https://www.gvhdalliance.orgThank you to our sponsors. This season is supported by a healthcare contribution from Sanofi  https://www.sanofi.com/ National Bone Marrow Transplant Link - (800) LINK-BMT, or (800) 546-5268.nbmtLINK Website: https://www.nbmtlink.org/nbmtLINK Facebook Page: https://www.facebook.com/nbmtLINKFollow the nbmtLINK on Instagram! https://www.instagram.com/nbmtlink/The nbmtLINK YouTube Page can be found by clicking here.To participate in the GVHD Mosaic, click here: https://amp.livemosaics.com/gvhd

Chuck Ryan from MSKCC joins to talk about various aspects of AR inhibition in prostate cancer and relative benefits and risks.

What are we to make of this large RCT of extended vs standard pelvic lymph node dissection (PLND) for prostate cancer?? Despite it not meeting its primary endpoint of improving biochemical recurrence, the authors now report in European Urology that it does reduce the incidence of distant metastases 10 years later! Go figure! We chat with Dr Karim Touijer (MSKCC) and try to figure it out. We ask about data dredging, p-hacking and statistical shenanigans, and how adding two minutes and two extra lymph nodes to a PLND could possibly lead to reduced metastases. Plus guest comments from Dr John Yaxley (Brisbane). What do you think??!! Will this change practice?? Will this change guidelines? Tune in and share your thoughts!Even better on our YouTube channelLinks:Paper in European Urology Previous GU Cast with Karim discussing earlier paper (Feb 2022) 

Dr. Doris Ponce from Memorial Sloan Kettering Cancer Center delves into atypical presentations of chronic graft-versus-host disease (cGVHD). As an associate member, co-chair of the Center for Hematologic Malignancies, and director of the Graft-Versus-Host Disease Program, Dr. Ponce provides an in-depth understanding of this complex condition.Dr. Ponce emphasizes the diverse symptoms of GVHD that often overlap with other conditions, making diagnosis challenging. She outlines the eight organs typically affected by GVHD: skin, mouth, eyes, musculoskeletal, genitourinary, lungs, liver, and gastrointestinal tract. However, she highlights that GVHD can also present atypically in organs such as the kidneys, nervous system, muscles, heart, and pancreas, causing symptoms such as serositis, effusions, nephrotic syndrome, and autoimmune disorders like vitiligo.Atypical presentations of GVHD are rare and require exclusion of other conditions such as drug side effects or infections before diagnosis. Dr. Ponce stresses the importance of patients communicating any new or unusual symptoms with their clinicians, as these might not initially seem connected to GVHD.Focusing on skin-related GVHD, Dr. Ponce describes common and atypical manifestations, including tight skin (sclerodermatous changes), pigmentation loss, dryness, and psoriasis-like appearances. Treatment varies but often involves topical steroids or immune suppression tailored to individual symptoms. For daily skincare, she advises avoiding frequent hot showers, using lukewarm water, and selecting gentle, fragrance-free products to prevent skin irritation.Regarding sun exposure, Dr. Ponce recommends using broad-spectrum sunscreen with SPF 30 or higher, and wearing protective clothing to prevent rashes exacerbated by sunlight. She also discusses the use of chemical and mineral sunscreens, noting that mineral sunscreens, despite being thicker, are better suited for sensitive skin.Peggy and Dr. Ponce discuss the Long Good Feel Better program that the American Cancer Society provides. For patients wanting to wear makeup, Dr. Ponce suggests choosing products designed for sensitive skin, avoiding those with harsh ingredients or multiple components, and replacing makeup regularly to prevent contamination. She also warns against using organic or preservative-free makeup due to infection risks.Haircare after GVHD often involves managing hair loss and changes in texture. Dr. Ponce advises infrequent washing, using gentle products, and considering supplements like biotin. For wigs, she cautions against those requiring glue and suggests alternatives like clip-on wigs or scarves. Hair dyeing is permissible with ammonia-free products.Nail care post-transplant includes using nail hardeners and avoiding acrylic nails. Dr. Ponce also emphasizes checking for underlying issues like vitamin deficiencies that may affect nail health.In closing, Dr. Ponce highlights the holistic approach to patient care at Memorial Sloan Kettering Cancer Center, addressing both medical and psychological aspects to support patients' overall well-being. She encourages patients to communicate any concerns, as seemingly minor symptoms might significantly impact their health and recovery. Dr. Ponce's dedication to improving patients' lives extends beyond treating their conditions, fostering confidence and quality of life throughout their recovery journey.More:Memorial Sloan Kettering Cancer Center's Tips for Managing GVHD (created by Dr. Ponce and dermatologist) Dr. Alina Markova:https://www.mskcc.org/cancer-care/patient-education/tips-managing-graft-versus-host-disease-gvhdAmerican Cancer Society's Look Good Feel Better Program: https://lookgoodfeelbetter.org/Memorial Sloan Kettering Cancer Center Website: https://www.mskcc.org/Sally Hansen Nail Hardener: https://www.sallyhansen.com/en-us/nail-care/nail-care/mega-strength-hardenerSurvivor recommended clothing brands that have SPF/UPF clothing:Coolibar: https://www.coolibar.com/Columbia: https://www.columbia.com/c/sun-protection/Baleaf: https://www.baleaf.com/collections/upf50This season is made possible thanks to donations from Syndax and Incyte.https://syndax.com/https://incyte.com/ Follow the nbmtLINK on Instagram! https://www.instagram.com/nbmtlink/

Dr. Diane Reidy-Lagunes is a top NYC Oncologist from Memorial Sloan Kettering Cancer Center. She is the creator and host of the award-winning monthly podcast Cancer Straight Talk from MSKCC where she leans in and tackles the subject of cancer head on, in English and Spanish. A noted clinical investigator, Diane served previously as President of MSK's Medical Staff. She currently serves as Vice Chair in the Department of Medicine. During the COVID crisis in NYC, she served as Chief of Clinical Care as part of the Hospital Incident Command System. As a researcher, she focuses on developing treatments of gastrointestinal (GI) tumors. She is a member of the National Cancer Institute Taskforce and a member of the National Cancer Care Network Guidelines. She is the recipient of several honors, including the Paul Sherlock Teaching Award, Castle Connolly Top Doctors, and the American Cancer Society Mother of the Year Award. In addition, Diane maintains a high-volume GI Oncology clinic.You can find her podcast Cancer Straight Talk at https://www.mskcc.org/cancerstraighttalk. This episode is part of a special series in collaboration between The Fiftyfaces Podcast at fiftyfaceshub.com and The Mindshare Podcast at www.monumentalme.com/podcast. --- Support this podcast: https://podcasters.spotify.com/pod/show/mindshare/support

Podcast Description: In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Mueller and Manning-Geist to discuss molecular classification in ovarian preservation for uterine cancer. Jenny Mueller MD is a gynecologic oncologist and an associate attending in the department of surgery at Memorial Sloan Kettering Cancer Center.  She leads the endometrial cancer research team at MSKCC with an emphasis on prospective, translational and collaborative efforts within and across institutions. Beryl Manning-Geist is a Gynecologic surgery fellow at Memorial Sloan Kettering Cancer Center and will be joining Emory University Division of Gynecologic Oncology in 2024 as an assistant professor. Her research focuses on how to leverage the molecular underpinnings of gynecologic cancers for tailored treatment. Highlights: -Patients with microsatellite instability-high/mismatch repair-deficient or copy number-high/TP53abnormal endometrial cancer were at increased risk of concurrent ovarian disease. -The presence of lymphovascular space invasion and positive cytology were also associated with an increased risk of concurrent ovarian disease. -Integrating molecular tumor profiling with pathologic characteristics of disease may help to better risk stratify pre-menopausal patients with endometrial cancer for ovarian preservation.

In a conversation with CancerNetwork® at Memorial Sloan Kettering Cancer Center (MSKCC), Neil M. Iyengar, MD, spoke about developments and challenges in his career as a medical oncologist and clinical investigator as well as ongoing research efforts in improving outcomes among patients with breast cancer.  Iyengar, a breast oncologist in in the Department of Medicine at MSKCC and Weill Cornell Medicine in New York City, New York, as well as the co–editor-in-chief of the journal ONCOLOGY®, detailed his work in the emerging field of exercise oncology. Based on preclinical data supporting the potential anti-tumor effects of exercise, he and his colleagues are organizing several clinical trials to validate whether exercise intervention can improve cancer-specific end points. Although some findings may support implementing exercise as part of a cancer treatment plan, Iyengar noted the observational and self-reported nature of the prior data and said that it would be necessary to test exercise intervention in the same way “you would develop any new drug for treating cancer.” Additionally, Iyengar discussed the fulfillment of ensuring patient care, a passion that has fueled his interest in lifestyle interventions such as exercise oncology. He highlighted how his cancer treatment philosophy extends beyond the goal of reducing tumor volumes to safeguarding the patient's physical and emotional well-being. “You can certainly hammer away at a tumor and give all kinds of chemotherapy and anti-cancer therapies, but if that [patient] is feeling miserable and has no quality of life and a short duration of response to that therapy, that's not necessarily the type of outcome that I would consider to be successful,” Iyengar said. “If you're able to either control or cure a cancer while also improving a [patient's] quality of life and general well-being, that's the kind of outcome that I strive for. When I see that in my patients and in the patients of my colleagues, that certainly brings a lot of fulfillment.” Iyengar also highlighted how he found excitement and passion in off-hours responsibilities to help achieve work-life balance. Looking ahead, he spoke about data on anti-estrogen agents, antibody drug conjugates, and other breast cancer treatment strategies that he is looking forward to hearing at the 2024 American Society of Clinical Oncology (ASCO) Annual Meeting.

Marcel van den Brink, MD,  is the Head and Alan N. Houghton Chair of the Division of Hematologic Oncology at Memorial Sloan Kettering Cancer Center. He is internationally renowned for his work in the field of bone marrow transplantation, the gut microbiome, and immunotherapy. He is also the Co-Director of the Parker Institute for Cancer Immunotherapy and Chairman of the Board of DKMS, an international nonprofit organization devoted to bone marrow donor registration. He is a recipient of numerous prestigious awards and is a member of the American Society for Clinical Investigation and he has been elected to the Royal Netherlands Academy of Arts and Sciences for his contributions in the field of hematologic malignancies. “Finding solutions is often as simple as shutting up and listening to what people formulate as the problem and what they have thought of as the answer. Without fail, I'm surprised that they've got something better than I could have come up with.” Join us in this episode of The Medicine Mentors where Chairman of Heme Malignancies at MSKCC, Dr. Marcel van den Brink, shares tips of effective leadership. Tune in as we learn about the five-minute ‘no talking, only listening' rule at the start of meetings and why the best leaders find comfort in not knowing everything. Pearls of Wisdom:   1. We will be leaders before we know it, and the simple formula of leadership is listening. When we conduct meetings, all we have to do is be quiet for the first five minutes and listen. 2. To know when we are ready to move on to the next stage, the next level, we have to know what we don't know, that is, do we know how to prioritize what matters, and if not, are we ready to seek help for it? 3. Failure and success often follow a 9:1 ratio, and so, to increase our chances of success, we should try our hands in different endeavors to see where we can truly shine. 4. Just like listening is the pathway to leadership, respect is the pathway to teamwork, and we should be mindful of it in our day-to-day interactions.

Michael Offin, MD, MSKCC, joins us for an informative session about chemotherapy drugs, their uses, side effects, and supportive medications.

JCO PO author Dr. Amit Mahipal shares insights into his JCO PO article, “Tumor Mutational Burden in Real-world Patients with Pancreatic Cancer: Genomic Alterations and Predictive Value for Immune Checkpoint Inhibitor Effectiveness.” Host Dr. Rafeh Naqash and Dr Mahipal discuss real world evidence of immune checkpoint inhibitors in pancreatic ductal adenocarcinoma. TRANSCRIPT Dr. Rafeh Naqash: Welcome to JCO Precision Oncology Conversations, where we bring you engaging conversations with authors of clinically relevant and highly significant JCO PO articles. I'm your host, Dr. Rafeh Naqash, Social Media Editor for JCO Precision Oncology and Assistant Professor at the OU Health Stephenson Cancer Center, University of Oklahoma. Today we are joined by Dr. Amit Mahipal, Professor of Medicine and Director of GI Oncology at the Case Western Reserve University in Seidman Cancer Center. Dr. Mahipal is also the author of the JCO Precision Oncology article titled "Tumor Mutational Burden in Real World Patients with Pancreatic Cancer: Genomic Alterations and Predictive Value of Immune Checkpoint Inhibitor Effectiveness."  Our guest disclosures will be linked in the transcript. For the sake of this conversation, we will refer to each other using our first names. So Amit, welcome to our podcast and thank you for joining us today. Dr. Amit Mahipal: Thanks for having me here. Dr. Rafeh Naqash: Excellent. We came across your article in JCO Precision Oncology and it really aroused my interest because the topic and the audience that it caters to is very important in the current times. Because immunotherapy generally is considered- pancreas cancer the graveyard in immunotherapy in essence, based on what I have seen or what I have encountered. And now you're the expert here who sees people with pancreas cancer or has done a lot of work in pancreas cancer research side. So can you tell us the context of this work and why you wanted to look at immune checkpoint inhibitors in pancreas cancer? Dr. Amit Mahipal: Absolutely, Rafeh. As you mentioned, pancreatic cancer is considered a what we call "cold tumors." They don't typically respond to immunotherapy. And when we talk to our patients or patient advocates, as you know, patients are very excited about immunotherapy. Immunotherapy has transformed the treatment for a lot of different cancers and not only has increased survival, but the quality of life is so much different than with chemotherapy. This work came from based on the KEYNOTE-158 trial, which was a tumor-agnostic trial which accrued patients who had TMB high tumor. What that means is that tumor mutation had more than 10 mutations per megabase. And what happens is because of that trial, more than 200 patient trial, the FDA actually approved this immunotherapy or pembrolizumab as a single agent pembrolizumab for any patient with a solid tumor who has high TMB. Again, tumor mutation burden, more than 10 mut/Mb. This question comes in now. Does this apply to our pancreatic cancer patient groups? Especially as we know these are "cold tumors" that typically do not respond. There have been multiple trials looking at immunotherapy, single agent, dual immunotherapy agents, as well as combinations with chemotherapy, with somewhat very, very limited success. So that was kind of the basis. So we wanted to look at this retrospective kind of review of a big database to see how many patients we can find who have high TMB and see in that patient population is immunotherapy really active based on the FDA approval or is pancreatic cancer not a tumor where we should try immunotherapy unit as a selective group.    Dr. Rafeh Naqash: Thank you for that explanation. Taking a step back again, since you see these individuals with pancreatic cancer I imagine day in and day out in the space of drug development, what is the general current standard of care approach for individuals with pancreas cancer in your clinic? I'm talking about what are the most common approaches that you utilize that seem to be working or have FDA approvals in the pancreas cancer space. Dr. Amit Mahipal: As with any tumor, the first thing is obviously staging. So depending on whether we're dealing with early stage or advanced stage and what are the goals of treatment. At this point, the only thing that can cure pancreatic cancer patients that would be considered conventional therapy is surgical resection. So any patient who is a candidate for surgical resection is in a different bucket compared to advanced patients. For early stage patients, we try to do what we call neoadjuvant treatment or neoadjuvant chemotherapy. We shrink the tumor or at least maintain it, look at the biology of the disease, and then take them to surgery, which typically involves a Whipple procedure if it's a head of the pancreatic mass.   Moving on to advanced patients, that's where we know the goal of treatment is palliative to increase survival, but unfortunately, most of the times we cannot cure them. And there the standard of care options include systemic chemotherapy. We have two typical regimens that we use, one is called FOLFIRINOX, which is a three-drug regimen of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan. And another regimen is gemcitabine plus abraxane, which is a two-drug regimen of gemcitabine plus abraxane. These are considered the standard of care. Unfortunately, the median survival even with the best standard of care chemotherapy is only about a year, 12-13 months, depending on what trials we look at.  Dr. Rafeh Naqash: I still remember some of these regimens from my fellowship, where we had to decide which to give to each individual based on their performance status and clinical status, etc. But now I can see a lot of ongoing drug development in the space of pancreas cancer. I'm guessing that's why you wanted to assess both the molecular genomic landscape of pancreas cancer in this study and also look at the immune biomarker aspect. Could you tell us a little bit about the Foundation Medicine Clinical Genomic Database? How did you identify the patients, how many patients did you identify, what you narrowed down in the criteria, and the eventual sample size of what you were looking at?  Dr. Amit Mahipal: FoundationOne has a rich database. They have two or three things. One is a genomic database only. So in our clinical practice, I think it's some sort of next-generation sequencing or mutational testing for all patients with advanced solid tumors. All of these goes into their database. All of the samples that are sent to FoundationOne that goes into their database where they know the diagnosis of the patient and the know the sequencing results of these patients. In addition, they also have a clinical database called Flatiron. Basically, they collaborated with them. Flatiron has about 280 or so cancer clinics throughout the country, so a lot of community settings and some academic sites as well. They did not only have a genomic database, but they actually have a clinical database. They have demographics, clinical features, baseline clinical features, comorbidities, what kind of treatment they received, what would be the stage of the cancer, how many months of treatment they received, and their overall survival, and so on. So from that perspective, the FoundationOne has access to this partnership with Flatiron, clinical genomic database where they have both clinical data as well as genomic database for a lot of these patients.  In our study, we only focused on patients with advanced pancreatic cancer. We excluded a lot of patients who did not have sequencing results available, they cannot be performed due to lack of tissue. So the first we talked about the genomic database and we found about about 21,932 patients, so almost 22,000 patients and there we had the sequencing and we also had the data on TMB or tumor mutational burden. So here, we classified them into two groups: high TMB and low TMB. High TMB was seen in 1.3% of the patients, and about 98.3% of the patients had low TMB. Here we looked at the genomic alterations between the two groups. So these are like our genomic group, so to speak of about 22,000 patients. And among them, as mentioned, that the clinical data was available for about 3300 patients or 3279 patients to be exact.   After excluding some of those patients, we found about 51 patients who received immunotherapy. And when we say immunotherapy, it is single agent immuno checkpoint inhibitor like pembrolizumab or nivolumab. And then we classified them into high TMB versus low TMB and then we also looked at patients with high TMB and compared them to who received immunotherapy versus other therapies. Just to recap, we had about 22,000 patients where we have the genomic database and about 3300 or so patients who we have both genomic and clinical data for this patients. One of the key findings was that high TMB was present in only 1.3% of the patients, or about 293 patients out of 21,932.  Dr. Rafeh Naqash: Definitely an interesting sample size that you had utilizing this resource, which, of course, is more or less real-world. It is important to gather real-world outcomes that you did.   So, going to the TMB story of this paper, where you looked at immune checkpoint inhibitor use in these individuals, was there a reason why some of the individuals with low TMB were also given immune checkpoint inhibitors? From my understanding, I did see some checkpoint inhibitor use there. What could be the explanation for that? Dr. Amit Mahipal: So this data is from 2014 to 2022. So from the span of about eight or so years. And as you know, immune checkpoint inhibitors were approved in the last decade. And there were a lot of not only trials, but even in the non-trial setting, people had tried immune checkpoint inhibitors in, frankly, different tumor types because of the success in some of the common tumor types, like melanomas, lung cancer, and so on. So I agree, as of today, we probably would not use immune checkpoint inhibitors in patients with low TMB or MSS. But at that time, I think that information was not available. So people with low TMB and MSI-stable tumors also received immune checkpoint inhibitors. But those numbers are again low. So it's not very high numbers. Dr. Rafeh Naqash: Understandable. That makes it a little more clear.  Now, you looked at the TMB aspect. I'm guessing you also looked at the MSI aspect of PDAC. What is your understanding, or what was your understanding before this study, and how did it enhance your understanding of the MSI aspect of PDAC? And I'm again guessing, since TMB high individuals are on the lower side percentage, so MSI high is likely to be low as well. Did you see any interaction between those MSI highs and the TMB highs on the PDAC side?  Dr. Amit Mahipal: Yeah, absolutely. So we are very excited in general about MSI-high tumors for solid tumors because of their response to immunotherapy. Although I would do a caveat because we still don't know how MSI-high pancreatic cancer responds although there have been some real-world, very, very small series as well. In this study, one of the things is, is high TMB totally driven by MSI-high? That's a question that comes up, and TMB high may not matter. It's only the MSI-high that might matter. So definitely when we look at this patient population, we found that the patients who were 35-36% of patients who were TMB high also had MSI-high patients. So we do expect MSI-high patients to have a higher TMB compared to MSS patients. But there were about 66 or two-thirds of the patients who did not have MSI-high tumors and still had high TMB, as defined by, again, ten mutations per megabase. So we did see patients with MSI-stable tumors who had high TMB. And I think that was one of our biggest questions. I think MSI-high patients, we all tend to think that we would try immunotherapy even if it's in pancreatic cancer. I think what is not clear, at least from the real-world or any of the trial data, is if we were to give MSI-stable patients who have high TMB, if we give immunotherapy, are there any responses or any disease control that we see? And that was one of the reasons for this study.  Dr. Rafeh Naqash: Now, one of the things that comes to mind, and again, I think you based it on the FDA approval for TMB high, which is ten mutations per megabase, as you defined earlier. I do a lot of biomarker research, and oftentimes you come across this aspect of binary versus a linear biomarker, in this case being TMB, where about ten, less than ten. Do you think, in general, an approach where you maybe have tertiles or quartiles or a biomarker, or perhaps a better approach in trying to stratify individuals who may or may not benefit from immunotherapy? Dr. Amit Mahipal: That's a great point. I think when we use ten mutations per megabase as a biomarker, as a binary endpoint, do we apply it to all tumor types? I don't think that's a fair comparison, frankly speaking. We do know that high TMB, even in different tumor types, do tend to respond a little bit better to or do have better outcomes for patients treated with immune checkpoint inhibitors in different tumor types. But what that cutoff is not known in most of the tumor types. And also, one of the problems is how do you measure TMB and is it standard across different platforms? Like I'm just giving some names like FoundationOne, Tempus, Caris, and some obviously like MSKCC and some other university-owned panels as well. And frankly, I think if you look at different panels and if you send the same tumor tissue, you will get different measurements. So I think standardization is a problem as well.  In one of the studies involving cholangiocarcinoma, for example, we found that a TMB of 5 was enough to have an additive effect of immunotherapy, same with chemotherapy, so to speak. But again, this needs to be validated.  So you're absolutely correct. I don't know why we use the binary endpoint, but on the same token, the binary endpoint is easy to understand as a clinician. Like, “Hey, someone has this, do this, not this.” And when we look into a continuous range, I think the benefit obviously varies between high and low, different tertiles, and becomes somewhat challenging. How do you classify patients and what treatments to give? So I think in clinical decision-making, we like the cutoffs, but I think in reality, I don't know if the cutoff is a true representation. And maybe with the more use of AI or computing, we can just input some values, and then it can tell us what the best treatment option might be for the patient. But that's way in the future. Dr. Rafeh Naqash: That would definitely be the futuristic approach of incorporating AI, machine learning perhaps, or even digital pathology slides in these individuals to ascertain which individuals benefit.  Going back to your paper, could you highlight some of the most important results that you identified as far as which individual is better, whether it was immunotherapy, and you've also looked at some of the mutation co-mutation status. Could you highlight that for our listeners? Dr. Amit Mahipal: So the first thing we looked at was the genomic database of almost 22,000 patients, and then we classified them into high TMB and low TMB, with about 300 patients in the high TMB group and the rest in the low TMB group. And what we found was, talking about again in the genomic database, that patients who have high TMB actually have low KRAS mutation. So if we think about KRAS mutation, pancreatic cancer, almost 85% or so of patients have KRAS mutation who have pancreatic adenocarcinoma. So patients in this subgroup, so in the high TMB group, only about two-thirds of the patients had KRAS mutation, compared to 92% of the patients with low TMB who had KRAS mutation. So just giving that perspective. So KRAS mutation, which is the most common mutation in pancreatic cancer and is a driver mutation, their rates vary differ from the high TMB group versus the low TMB group.   And then in addition, in the high TMB group, we found higher rates of BRCA mutation, BRAF mutation, interestingly, and then obviously from the DNA damage repair genes like PALB2 mutation, MSH2 or MSH6, MLH1, and PMS2. So all these mismatch repair protein mutations were higher. As I mentioned before, one-third of the patients with high TMB also had MSI-high. So it's not a totally unexpected finding. I think the biggest finding was that we found more KRAS wild-type pancreatic adenocarcinoma in the high TMB group, almost a third. And those tend to have different targetable mutations like BRCA2, BRAF, and PALB2 mutations. So I think one of the interesting findings is that patients in the high TMB group actually tend to have KRAS wild-type or less KRAS mutations. So they're not necessarily KRAS-driven tumors, and they have a higher chance of having other targetable mutations like BRAF and so on, for which we have therapies for. So it's always something to keep in mind. Dr. Rafeh Naqash: Would you think that from a DDR perspective, the mutations that you did  identify that were more prevalent in individuals with high TMB, do you think that this is linked to perhaps more DNA damage, more replication stress, more neoantigens leaning toward more tumor mutation burden perhaps? Or is there a different explanation?  Dr. Amit Mahipal: For sure. As we said, MSI-high tumors have mutations in the DNA damage repair pathway and they definitely tend to have higher TMB. So I don't think that is very surprising that we found PALB2, or other MMR genes like MSH2, MSH6, MLH1, and PMS2 at much higher rates. I think the interesting finding is the fact that the KRAS wild-type and having BRAF alterations at least that's not suspected to definitely increase TMB. Although if we look at colorectal cancer, BRAF mutation and MSI are somewhat correlated to patients with BRAF mutations and to have high rates of MSI-high tumors. But that's not the case in pancreatic cancer. We also found an increase in BRCA2 mutations as well. So I agree that the DNA damage pathway repair gene alteration is not unexpected because they tend to increase TMB, but I think the other mutations were interesting. Dr. Rafeh Naqash: And I think one other aspect of this, which I'm pretty sure you would've thought about is the germline implications for some of these mutations where you could very well end up screening not only the individual patient, but also their family members and have measures in place that we're trying to enhance screening opportunities there. In your current practice, you are at an academic center but I'm talking about in general with your experience, how common is it to sequence broad sequencing panels in individuals with pancreas cancer? The reason I asked that is I do a lot with lung cancer and even now despite having all those targets in lung cancer which sort of paved the pathway for targeted therapy in many tumor types, we still don't see a full uptake for NGS Phase I drug development. And I get a lot of referrals from outside and I often see that it's a limited gene panel. So what is your experience with pancreatic cancer? Dr. Amit Mahipal: We kind of changed our practice. Similar to you, I'm involved in drug developments. I've been a big proponent of NGS for almost a decade now, when didn't even have targeted therapies but these companies first came in and they're like, “Okay. We're very very low chance.” But now obviously, we transformed the treatment for a lot of different cancers. Especially lung cancer, you don't sometimes even start treatment before you get an NGS panel like you said in situ. So what we're finding, at least for pancreatic cancer, as you know, the targetable mutations are there but they are somewhat not that common, I would say, in the 10-15% range. So many people would get dissuaded and then it's like, what's the point of doing it?   But I think for those 10% to 15% of the patients, firstly we can really change their treatment course and their prognosis. Secondly, if you don't do it and they cannot go in a different clinical trials, now we have trials targeting KRAS G12C, but not only that, KRAS G12D which is the most common mutation we see in pancreatic cancer and so on. So it's becoming very very important. One thing, at least with our practice we adopted last two or three years is sending liquid biopsies or liquid based NGS or blood-based NGS testing. Otherwise, what's happening I would send a solid tumor NGS from the tissue. And pancreatic cancer as you know has sometimes a very small amount of tissue obtained from FNA. And inevitably after four weeks, we'll get the result that there's not enough tumor to do NGS testing. And then the patient comes one or two months later and then we order the test, and that just delays everything.  So now we adopted a practice where we are trying to send both blood based NGS and solid tumor NGS at the same time the first time of diagnosis when we see the oncologist for the first time. And that has really increased the rate of NGS testing results for our patient population. And it's not 100%, even in blood-based NGS, sometimes they may not be able to find enough circulating tumor cells to do this blood-based NGS testing, but at least they're having these. But you're correct. I think we still see about one third of the patients who had not had NGS testing or referred for phase I clinical trial and have gone through more than two or three line of therapies which is unfortunate for our patients.  Dr. Rafeh Naqash: That's a very interesting perspective on how important it is to sequence these individuals. As you said, it may not be that all of them may benefit, but the ones that have those important alterations, especially BRCA, PALB, and KRAS could benefit from novel precision medicine-based approaches.  A question that came to my mind, I saw that you were trying to look at MYC and turmeric low tumors as well. So what is the role of MYC in the context of these individuals? Is there any drug development that's going on? Because I see small cell lung cancer. MYC is an important target there. These are two different tumors, but it looks like there was a hint of some correlation with respect to some of the findings that you showed. Is that something that you're currently looking at or planning to look at?  Dr. Amit Mahipal: I think that if we just talk about MYC in general, it is present at somewhat lower rate. I think we found MYC amplification in about 5% or so of TMB-low patients who had that and not really seen in the TMB-high patients. So right now, I am not aware of any trials targeting MYC in pancreatic cancer. But as you said, if it's successful in lung cancer, maybe that's when we can transform into the pancreatic cancer group. Dr. Rafeh Naqash: Of course we can all learn from each other's specialties.We learned a lot from melanoma with respect to therapy. Hopefully, other fields can also benefit from each other's experiences in the space of drug development.  Thank you so much for this interesting discussion. The last few questions are more or less about you as an individual researcher. So could you tell us briefly on your career trajectory and what led you into the space of GI oncology, pancreas cancer, even for that matter, drug development? And some of the advice that you may want to give to listeners who are trainees or early career individuals? Dr. Amit Mahipal: Sure. So I have gone through some different institutions. During my fellowship, that's when I really decided that I wanted to do GI oncology. Prior to that, I actually have a Masters in Public Health, where I learned about epidemiological research and how to design clinical trials, how to design cohort studies. My focus was on, actually there was somewhat a lot, but one of my mentors was working on colorectal cancer, and they had this huge database called the Iowa Women's Health Study Database of 100,000 patients. So that's where I started by clearly getting into colorectal cancer and GI cancer in general and how to learn from this database, how to mine these databases, how to do analyses, which seems easy but is actually quite complicated.  During my fellowship, I think the key to it is finding a good mentor during the fellowship. And I worked with one of the top GI oncologists in the country who's practicing. And I worked under her and learned a lot not only from the clinic side but also from the research perspective and how sometimes you'll come up with the ideas during the clinic itself.Like, “Hey, this patient had this and why aren't we looking into this.” And she would even do some of the therapies based on phase II trials and she was a part of a lot of these trials and learning from those experiences.  And following my fellowship, I joined Moffitt Cancer Center, where I led the phase I program there. So I was heavily involved in drug development programs, all training programs I've been to, NIH in Bethesda, an observership in the CTEP program, and also did the ASCO/AACR Vail workshop, where you really learned a lot in just like one week. So those are kind of opportunities present for fellows and even the early investigators and attendings as well in the first few years can go there, have your proposal. And really they are the world experts in trial design and they'll talk about how to design trials, how to add collaborators, improve your trial, and basically learn the whole protocol in a week so to speak.   And then I was at Moffitt Cancer Center for about five, six years. My home was GI so I did both GI oncology as well as phase I. And in terms of the GI oncology, my main focus was pancreatic cancer and liver tumors. Then I was at Mayo Clinic in Rochester for about seven or so years. I kind of did the same thing and solidified my career at GI oncology, looking at liver tumors, and pancreatic cancer and then being a part of the phase I division program. And now, most recently, about a year or so ago, I joined Case Western to lead the GI program here. Dr. Rafeh Naqash: Are the winters in Cleveland better than the winters in Minnesota? Dr. Amit Mahipal: For sure. I always say, you don't know cold until you go to Minnesota. It's a different kind of cold. I'm sure people in Dakota might say the same thing, but the cold in Minnesota is very brutal and different compared to any other place I've been to.  Dr. Rafeh Naqash: Well, it was great learning about you. Thank you so much for spending this time with us and for sharing your work with our journal. We hope you'll continue to do the same in the near future.  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 ascopubs.org/podcasts. Dr. Amit Mahipal: Thank you for having me here, Rafeh. Good luck. Take care. Dr. Rafeh Naqash: Thank you so much. The purpose of this podcast is to educate and inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions.   The guests on this podcast express their own opinions, experiences, and conclusions. Their statements do not necessarily express the opinions of ASCO. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement.   Dr. Mahipal: Consulting or Advisory Role:QED TherapeuticsAstraZeneca/MedImmuneTaiho Oncology Speakers' Bureau:AstraZeneca Research Funding:Taiho Pharmaceutical"

A perennial topic on GU Cast!! But today we welcome a couple of very useful papers in European Urology Oncology which help us understand how PSMA PET/CT can help patient selection for pelvic lymph node dissection in prostate cancer. We are joined by Dr Giorgio Gandaglia from San Raffaele Hospital in Milano to discuss these two papers (links below). We also hear about Declan's recent trip to San Raffaele as Visiting Professor, and he sits down for a wide-ranging chat with professor Francesco Monitorsi, Director & Professor of Urology at San Raffaele. Even better on our YouTube channelLinks:Can PSMA reduce PLND? A systematic reviewOptimal use of PSMA to select patients for PLND. Updated validation of the Briganti and MSKCC nomograms

Dr. Shannon Westin and her guests, Dr. Judy Garber and Dr. Geoffrey Oxnard, discuss the paper "Germline EGFR Mutations and Familial Lung Cancer" recently published in the JCO. TRANCRIPT The guest on this podcast episode has no disclosures to declare.   Shannon Westin: Hello, and welcome to JCO After Hours, the podcast where we get in-depth on articles that are published in the Journal of Clinical Oncology. I am your host, Shannon Westin, Social Media Editor for the JCO and Gynecologic Oncologist by trade. And it is my great pleasure to speak today with you about an amazing manuscript entitled, “Germline EGFR Mutations and Familial Lung Cancer.” It was published in the JCO on August 14, 2023.  The authors have no conflicts of interest, and they are Dr. Geoffrey Oxnard, he's a Thoracic Oncologist and Associate Professor, Hematology and Medical Oncology at Boston Medical Center.  Welcome, Geoff. Dr. Geoffrey Oxnard: Hi, Shannon. Thanks. Shannon Westin: And Dr. Judy Garber, the chief of the Division of Cancer Genetics and prevention at the Dana-Farber Cancer institute in Boston. Welcome, Judy. Dr. Judy Garber: Thank you. Hi, Shannon. Hi, Geoff.  Shannon Westin: So excited you both could be here. Let's get started. So first I just want to levelset for our audience. Can you speak just a little briefly about the incidence and mortality of lung cancer and how that's been changing over time? Dr. Geoffrey Oxnard: Sure. Lung cancer is common and it's deadly, more than 200,000 cases a year in the United States, more than 100,000 deaths a year in the United States. But I think importantly, it's evolving. Its biology is evolving as smoking incidence goes down. We've identified these genomic subtypes of lung cancer that are sort of increasingly apparent and important as we think about its treatment. Outcomes are changing with emerging therapies, presentation is changing with lung cancer screening and with a growing ability to now find cancers early and prevent them. And so it's in that setting of a very dynamic disease that we chose to study a really unique little slice of it, which is germline risk. Shannon Westin: So let's take that one step further because I think that's really interesting. You mentioned the genomic aberrations and kind of how you're using that to target. Can you expand upon that a little bit more for me? Dr. Geoffrey Oxnard: Lung cancer that I've long studied is different than breast cancer when Judy has long studied because we think about its somatic alterations, we've always thought about KRAS mutations, EGFR mutations, and smaller and smaller splice limit. ALK, RAS, RET HER2, etc. And so tumor testing in lung cancer has one of the first to be standard across on solid tumor oncology. And the germline genetics was kind of an afterthought and is the flip, I think, of how genetic testing evolved in the breast cancer space for example. Dr. Judy Garber: I might argue a little bit if breast cancer was earlier and it was subtyped some molecularly it doesn't have as many molecular subtypes yet perhaps as lung cancer. But we've all been studying the somatic space to look for targets for therapy. And the germline space, certainly in breast cancer, came much earlier. And everybody knows about BRCA1 and 2. Now, we hope everybody knows about Lynch Syndrome, but certainly not everybody's thinking about inherited lung cancer risk. Dr. Geoffrey Oxnard: Yeah, these have converged. I think 10 years ago when this kicked off, I felt like a super outlier for thinking about, wait a second, what about the genetics behind all this that is leading to this strange variable presentation of lung cancer? For example, we know that in Asian populations, one type of lung cancer, EGFR mutant lung cancer, is more common. There must be some geneticness that leads to that. What explains the sort of pattern of presentation of these genetic subtypes in the populations we see in the US, that's pretty unclear?  Dr. Judy Garber: So, I think, Shannon one of the clues about all this came from the fact that the EGFR mutations were being identified in the tumors. And then I really should let Geoff tell this story, but as the amateur thoracic person in the room here, to me, it was so interesting that there were the EGFR mutations, then there was treatment exploiting EGFR mutations, and the most common resistance mutation was this T790M variant. But when labs started testing EGFR, there was a small group of people who had that resistance variant without ever having been treated at all. So that was the obvious question, what was it doing there? And that's where Geoffrey came in.  Dr. Geoffrey Oxnard: Yeah, this is a patient I met more than a decade ago at my fellowship in MSKCC. She'd been living with a T790M mutation in her tumor for years and years and years. I was like, “Well, I don't understand. Why is this sitting there?” And she had this sort of slightly mysterious history of lung cancer in her family. And we realized, wait a second, this T790M was behind her cancer from the beginning, and in fact, might have been the basis of why she developed lung cancer. And so that actually motivated a career development award I submitted to the Conquer Cancer Foundation of ASCO, a grant I received, and that then led to a program that I led at Dana-Farber under Judy's mentorship, where over the past decade, we sort of focused in and studied this strange, rare syndrome, really to dig into inheritedness as a kind of different flavor of lung cancer genetics.  Dr. Judy Garber: Well, and now it's really a good time to think about this because we're recognizing there are younger cancers, colon cancer, like an epidemic, and lung cancers, and we're not sure how many of them are genetic or come from other exposures. Geoff talked about the differences in Asia, some of which are certainly genetic, some which may be environmental, especially in the lung, where that's such an issue. But trying to sort these things out, you have to be willing to think a little bit differently. And that was fun when Geoff came from the lung program, interested in the germline, we said, “Oh, we have to do this.”   Shannon Westin: Well, let's talk about what you did. I would love to hear and I know the audience would as well about the design of this study, so called INHERIT study. Very good name. I love a good name. This is a good one.   Dr. Geoffrey Oxnard: Yeah. So that stands for Investigating Hereditary Risk of T790M, INHERIT. I forget where we coined that. Let me give you a case example. A patient presents in his 40s. I remember this man. He has an EGFR mutation in his tumor. He has a T790M in his tumor as well. He had routine tumor testing that lung cancer patients were getting. And he says, “Oh, also, my brother had lung cancer in his 40s just a couple of years ago. He was a smoker, though. He never had genetic testing.” And so this patient we test on the study, we hypothesized that when patients present with T790M at diagnosis, that it would be a representation of an underlying germline EGFR mutation. Our hypothesis was that about 50% of the time T790M at diagnosis would be explained by a germline behind the doll. And that that could then empower families like this one to understand the kinds of lung cancer they're getting in their family, the kinds of treatment they should be getting, and the kinds of testing they should be getting to look for lung cancer at risk early on.   It really saddens me that in a family that doesn't know about this condition, the brother would never get testing and would never think that I might be getting or might never get testing, might not be disposed to getting testing, and might not realize there's a therapy available to target that EGFR mutation if he died young without even much treatment. But this individual, we tested his lung cancer, we found him a therapy, we put him on a pill therapy that could last a very long time. And so we set up a program with a consortium alchemy, the Addario Lung Cancer Medical Institute, where we enrolled at three sites, both at Dana-Farber in Boston, Vanderbilt, and Ohio State, with some motivated investigators there that we appreciate their collaboration.  But also, again, this is now more than 10 years ago, set up shop where people could enroll remotely, that if you found a T790M in your tumor, for whatever reason, you could reach out to the team at Dana-Farber centrally and get consented online and even get counseling. And this is one of the early ways of getting this remote participation. And you can imagine, over the course of the study, we quickly ran out of individuals at any given site, but that remote enrollment accelerated and really allowed us to get to the large population of remote study. Dr. Judy Garber: We were lucky that things were happening. The things you don't expect. So EGFR testing was not routine at that time. And the EGFR testing that had developed in Dana-Farber and NGH became standard of care at Dana-Farber so we were finding those patients, and then grew outside as well, at institutions and testing labs. And these people would somehow emerge so we were very lucky that we were able to set up remote testing. We could send and get a saliva sample and be able to test. Or these were people who got tested through their own doctors, found out they had this mutation and then went online and said, “Who knows anything about this?”  I would say that we and our amazing genetic counselors who spoke to all these patients, took their detailed family histories, got their other information, and were able then to really build out these cohorts so we can understand them. And to look at, for example, Geoff's question, it was really his question, “Why did we have such clusters in certain parts of the country? Could it be that there were the so-called founder mutations that somebody had this mutation and they spread their genes around so that they're around the country and that turned out to be true. Shannon Westin: It's so fascinating, and I love how you kind of almost crowdsourced getting these patients to you because I was mystified because it's such a rare aberration and you had so many patients. Let's talk a little bit maybe about your patient population and who volunteered, and is it reflective of kind of you do think, the general population? Dr. Geoffrey Oxnard: I want to give a shout out to the GO2 Lung Cancer Foundation. That really was a lot of the ‘rah rah', getting people to know about this, having some word of mouth and spreading the word. And so certainly there are physicians around the country that have been like found patients that I've got to know because they sent us patients to study over the years. We ended up getting germline testing on 141 individuals who presented eligible for testing because of either a relative or a mutation that was suspicious for inherited. Most of those were enrolled remotely, in the end, as you might expect. We found what you might expect, that this was Mendelian in its inheritance, that if you had a first degree relatives, they had 50% chance of having this. And so we sort of slowly built these pedigrees of individuals who once they were positive, would refer in their relatives and say, “Please go get testing. Let's describe our family and help understand our risk.”   It ended up boiling down to six individuals with a germline EGFR mutation from 39 different families. I remember one family where two different cousins presented separately to the program, not knowing each other was participating. And so, of course, there's not that many of these families around the United states, but we're really very lucky to have touched so many different individuals. What did we find? That if you had a germline EGFR mutation, your tumor almost always had an EGFR mutation. That really is the dominant biology of lung cancer that presents in these affected individuals, that it presents young, that the likelihood of developing lung cancer is around 55% by age 40 to 50. So it really is– I'm trying to make sure I'm quoting that right, actually, Shannon, I'm looking at the numbers here, but it was a really broad range of diagnosis.  We had a 28-year-old who was affected and an 83-year-old who was affected. I saw a family where the grandson had lung cancer, but his father and grandfather who had germline EGFR mutations, did not. So variable penetrance. Judy, of course, told me, “Geoff, this is the way families present. Come on, Geoff.” But other families, incredible penetrance– not everyone having lung cancer, many of them smoking, some of them not smoking. But for these families, what a sense of empowerment to say, “Oh, this helps explain what's going on in our family, why this is happening at a younger age.” And helps explain the therapies that we had some concern about giving these potent EGFR inhibitors originally, understanding every cell in their body has this EGFR mutation. Are we going to somehow cause toxicity? No. These potent therapies can be effective, can be tolerated, and can work for many years. So we really feel hopeful that we've described a syndrome that's out there that people see and that has a distinct presentation, a distinct treatment pattern, and a clear association with lung cancer risk. Dr. Judy Garber: And I think that now the opportunity is to say, can you find these people before they get their lung cancers? Some of them have abnormalities on scans. Think of it's like the APC, the polyposis coli of lung cancer. You can see these adenomas forming, but we can't really predict exactly who's going to develop tumor when. And that, I think, is a challenge that families have to help us with because we need to continue to identify some of these people who have not had cancer. They have children. They want to know what to tell them besides not smoking adamantly and maybe with some hopes that we're going to do some screening.  I am afraid there probably is not good data that EGFR inhibitors could be used for prevention, but it's tempting to think that way. So there's plenty of work to do still to sort out the questions. This is the nature of genetics. We often find inherited susceptibility and people want to know, “Well, why would I want to know? What am I going to do about it?” And here I would say, “We're going to figure out what's your risk more specifically, and how can we help reduce that risk, in addition to telling you not to smoke.” Dr. Geoffrey Oxnard: I do want to allude to Judy's comment about founder effect. I didn't tell you exactly about the presentation, but these families, first off, we only found germline EGFR mutations in Caucasian individuals and in black individuals, and it was mostly in the United States and in fact, enriched in the southeast United States. And don't get me wrong, we had enthusiastic participation from Vanderbilt. But still it seemed like there was more southeast United States prevalence. And even families I met in the Boston area would say, ‘Oh yeah, I have relatives going back to Arkansas.”   And so we ended up with a bit of a suspicion for this geographic enrichment, studying the genomes of these affected individuals, and in fact did find a very large region of chromosome 7 that was shared in more than 90% of the folks we tested, suggesting a founder effect in the southeast United States, probably white and black. And that goes back hundreds of years, maybe 200, 300, 400 years, as far as we can estimate, making me think that this is a fairly unique syndrome that we're seeing in North America, but actually may not be prevalent in other parts of the globe. Though we did identify a single individual in Australia, it might be a unique phenomenon in North America. Dr. Judy Garber: At least more common. But these days, people travel, so hard to know. Shannon Westin: I don't know if you've gotten a chance to do this - any other cancer type seeming to be associated with this mutation? Dr. Judy Garber: No, fortunately not. Shannon Westin: Okay, very interesting. And what about outcome? What was the association, or was there any association of these mutations with cancer related outcomes? Dr. Geoffrey Oxnard: I would say the survival of these cancers isn't that different than EGFR mutant lung cancers. If they get to effective therapy, they can live for years on therapy. If they don't, they can do quite poorly. One interesting finding is that they can present in a multinodular fashion that might be multiple primaries. And so you can kind of use an approach of eliminating individual clones. Sometimes it's been described these different tumors have different mutations, and so you might treat them like a stage IV lung cancer, but actually they lived for a long time because actually they had multiple stage I lung cancers, so it can present a little bit differently. And then we tried to collect CT scans on affected carriers who did not yet have lung cancer to see if they might develop lung cancer. It was not required on study, and it's sort of an area of future investigation. But as you can imagine, lots of lung nodules and certainly anecdotes of individuals where we found early precancers through the screening effort, motivating the investigation that Judy was alluding to. Dr. Judy Garber: I think this is what you expect in inherited predisposition that you have an earlier chance. So some of them are younger, not the 84-year-old, but that they could be younger, that they could have multifocal disease, that their biology could be different, but could be the same, maybe accelerated, maybe not. Some of these are slower. And I think that's why we're excited to be able to continue this work with the group at Dana-Farber.  Now, Jaclyn LoPiccolo is going to lead the INHERIT study, but much of the team is the same. And now the focus will be even more on trying to really quantify the risk and help think about prevention strategies and screening for these patients. It's a little tricky to want to do too much chest CT screening. On the other hand, there are lower dose CTs now, and we hope the guidelines will clarify the role of inherited risk. At ASCO this year there were a lot of talks about inherited lung cancer risk, but nothing is quite as well characterized as, I think, the T790M population. Shannon Westin: Well, thank you all so much. This was fascinating. I learned a ton and I know our listeners did as well. And thank you to our listeners. This was “Germline EGFR Mutations and Familial Lung Cancer.” Again, published in the JCO August 14, 2023. So go check it out and check out our other podcasts on the website or wherever you get your podcasts. Have an awesome day.  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.  

In this rebroadcast episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Jenny Mueller and Bill Zammarrelli to discuss molecular classification and risk stratification in endometrial cancer. Jenny Mueller, MD, is a gynecologic oncologist and assistant attending in the department of surgery at Memorial Sloan Kettering Cancer Center. She leads the endometrial cancer research team at MSKCC with an emphasis on prospective, translational, and collaborative efforts within and across institutions. Bill Zammarrelli, MD, currently works as a gynecologic oncology fellow at Memorial Sloan Kettering Cancer Center. He is a commissioned officer in the US Army and completed his residency at Walter Reed National Military Medical Center. His current research focuses on the genetics of endometrial cancer.    Highlights: --PORTEC-1 and GOG-99 risk classifications are discordant for stage I grade 3 endometrioid endometrial carcinoma (EEC). --Stage I grade 3 EECs of CN-high molecular subtype have a worse 3-year progression-free survival compared to non-CN-high molecular subtypes. --Molecular classification in combination with clinicopathologic factors may provide improved prognostic information.

Dr. Brandon Fields and Dr. Gary Luker interview Dr. Allison Applebaum about the Caregivers Clinic at MSKCC, her advocacy for family caregivers, and what radiologists can do to help. Taking Time to Recognize Caregivers. Luker. Radiology: Imaging Cancer 2023; 5(6):e230191 Dr. Applebaum's book

In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Dr. Dennis Chi. Dr. Chi is the incumbent of the Ronald O. Perelman Chair in Gynecologic Surgery, Deputy Chief of the Gynecology Service, and Head of Ovarian Cancer Surgery at Memorial Sloan Kettering Cancer Center (MSKCC).  He has been a faculty member at MSKCC since graduating from fellowship there in 1997.   Highlights: Dr. Chi discusses the evolution of gynecologic surgery and the current state of the field, talks about finding a niche in the planning of one's career, and outlines difficulties in planning a surgical trial along with ways to overcome them.

In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Mario Leitao and Andreas Obermair to discuss FIGO endometrial staging. Dr. Mario Leitao is currently an Attending Surgeon in the Department of Surgery at Memorial Sloan Kettering Cancer Center and a Professor in the Department of Obstetrics and Gynecology at Weill Cornell Medical College. He currently serves as Program Director for the Gynecologic Oncology Fellowship. Dr. Leitao is also the Director for the Minimal Access and Robotic Surgery Program in the Department of Surgery for MSKCC. Dr. Andreas Obermair is an active gynaecological oncologist in public and private practice and a Professor of Gynaecological Oncology at The University of Queensland in Brisbane, Australia. He leads the Queensland Centre for Gynaecological Cancer Research to achieve less invasive and more effective treatments for gynaecological cancer.   Highlights: The new FIGO (staging) system is no longer a staging system to determine the extent of endometrial cancer Histology and other prognostic factors should not be part of a staging system We need much more investigation and validation before we can apply a molecular classification to the care of our patients and then it should not be part of a staging system An international staging system is likely best if kept reproducible, and if it can be applied worldwide There is poor correlation now with this new system and the AJCC TNM system

Dr. Mohamed Soliman discusses mentorship in research with Dr. Sungmin Woo, director of GU imaging at MSKCC. 

Dr. Neeraj Agarwal and Dr. Jeanny Aragon-Ching discuss the CLEAR study in renal cell carcinoma, a new exploratory analysis combining the TheraP and VISION trials in metastatic urothelial cancer, and compelling advances in prostate cancer and across GU oncology in advance of the 2023 ASCO Annual Meeting.  TRANSCRIPT Dr. Neeraj Agarwal: Hello and welcome to the ASCO Daily News Podcast. I'm Dr. Neeraj Agarwal, your guest host for the ASCO Daily News Podcast today. I'm the director of the Genitourinary Oncology Program and a professor of medicine at the University of Utah Huntsman Cancer Institute, and editor-in-chief of the ASCO Daily News. I'm delighted to welcome Dr. Jeanny Aragon-Ching, a GU medical oncologist and the clinical director of the Genitourinary Cancers Program at the Inova Schar Cancer Institute in Virginia.   Today, we'll be discussing some key abstracts in GU oncology that will be featured at the 2023 ASCO Annual Meeting.  Our full disclosures are available in the show notes and disclosures of all guests on the podcast can be found on our transcript at asco.orgDNpod.   Jeanny, it's great to have you on the podcast today. Dr. Jeanny Aragon-Ching: Thank you so much, Dr. Agarwal, for having me. Dr. Neeraj Agarwal: Jeanny, let's begin with Abstract 4502 regarding long-term updated results on the CLEAR study. The abstract reports the final, prespecified overall survival analysis of the CLEAR trial, a four-year follow-up of lenvatinib plus pembrolizumab versus sunitinib in patients with advanced renal cell carcinoma. Dr. Jeanny Aragon-Ching: Yes, I would be happy to. So, just as a reminder, the combination of lenvatinib and pembrolizumab was initially approved by the FDA in August 2021 for first-line treatment of adult patients with advanced renal cell carcinoma. So, this was based on significant benefits that were seen in progression-free survival, which was a primary endpoint, but also showed improvement in the overall response rates compared with sunitinib in first-line advanced renal cell carcinoma.   So this abstract reports on longer-term follow-up now at a median of 49.8 months, and PFS favored the combination lenvatinib and pembrolizumab compared to sunitinib across all MSKCC risk groups, and PFS benefit versus lenvatinib and pembro compared to sunitinib was maintained with a hazard ratio of 0.47. And even overall survival was also maintained with the combination with a hazard ratio of 0.79, and the overall survival favored the combination across all risk groups. If we look at the CR rate, it was 18.3% for the combination compared to 4.8% with sunitinib, unless patients in the combination arm received subsequent anticancer therapies, and that's intuitive. And the PFS2 was also longer with the combination at 43 months compared to 26 months. Now, it is important to note that grade III or more treatment-related adverse events did occur in about 74% of the patients in the combination of lenvatinib and pembro, compared to 60.3% in patients with sunitinib. Dr. Neeraj Agarwal: Jeanny, this is good news. So the main message from the abstract is that sustained results from this combination of lenvatinib plus pembrolizumab are being seen even after a longer follow-up of more than four years.  Dr. Jeanny Aragon-Ching: Yes, I agree. So now, moving on, Neeraj, to a different setting in the RCC space, let's look at Abstract 4519, which is titled “Efficacy of First-line Immunotherapy-based Regimens in Patients with Sarcomatoid and/or Rhabdoid Metastatic Non-Clear Cell RCC: Results from the IMDC,” which will be discussed by Dr. Chris Labaki. So, Neeraj, based on this abstract, can you tell us a little bit more about the impact of these adverse pathologic risk features in non-clear cell RCC?  Dr. Neeraj Agarwal: Of course. So, using real-world patient data, the IMDC investigators compared the outcomes of patients with metastatic non-clear cell RCC who were treated with immunotherapy-based combination regimens versus those who were treated with VEGF-TKIs alone. They also assessed the impact of sarcomatoid and rhabdoid features on response to IO-based combinations versus VEGF-TKIs. Of 103 patients with metastatic non-clear cell RCC who had rhabdoid or sarcomatoid features, 32% of patients were treated with immunotherapy-based combinations.   After adjusting for confounding factors, the authors show that those treated with a combination of two immune checkpoint inhibitors or an immune checkpoint inhibitor with a VEGF-TKI combination had significantly improved overall survival, which was not reached in the immunotherapy combination group versus seven months within the VEGF-TKI group. Time to treatment failure and objective responses were also prolonged, significantly higher, and better in the immunotherapy groups compared with patients who were treated with VEGF-TKIs alone. Interestingly, if you look at those 430 patients with metastatic non-clear cell RCC who did not have sarcomatoid or rhabdoid features, they didn't seem to benefit with immunotherapy-based combinations.  Dr. Jeanny Aragon-Ching: This is an exciting update, Neeraj. What are the key takeaways from this abstract? Dr. Neeraj Agarwal: So the main takeaway is if you see a patient with advanced non-clear cell RCC who has sarcomatoid and rhabdoid features, there appears to be a rather substantial and selective benefit with IO-based combinations. And in this context, I would like to highlight the ongoing SWOG 2200 trial also known as PAPMET2 trial, which is comparing the combination of cabozantinib plus atezolizumab. So immuno-therapy-based combinations versus cabozantinib alone in advanced papillary renal cell carcinoma setting. So this trial is being led by Dr. Benjamin Maughan and Dr. Monty Pal. And I like to encourage our listeners to consider referring their patients for involvement in this federally funded trial so that we can validate the data from this retrospective study in a prospective way. So, Jeanny, let's now move on to another important disease type which is urothelial carcinoma. There is a very recent accelerated FDA approval of the drug combination of enfortumab vedotin and pembrolizumab for cisplatin-ineligible metastatic urothelial carcinoma patients. This is Abstract 4505, which is being presented by Dr. Shilpa Gupta and colleagues. Can you please tell us more about this update? Dr. Jeanny Aragon-Ching: Yeah, absolutely. So, as you mentioned, Neeraj, the FDA just granted accelerated approval in April 2023 for this combination of enfortumab vedotin or EV, which is and ADC, antibody drug conjugate against nectin-4 and the PD-1 inhibitor pembroluzimab. So it's a combination for patients with locally advanced or metastatic urothelial carcinoma who are considered cisplatin ineligible. So this is nearly a four-year follow-up.   So as a reminder, this was a phase 1b/2 trial that included 45 patients and it had a primary endpoint of safety and tolerability although the key secondary endpoints included confirmed overall responses, duration of response, progression-free survival, and the resist criteria was investigated via investigator and BICRs which is in a blinded independent central review. Even overall survival was a key secondary endpoint.  So, the bottom line was the confirmed overall response by BICR was 73.3%, the disease control rate was about 84%, and the CR rate was 15.6% with a PFS of close to 13 months, and a 12-month overall survival rate of 83%. However, it is important to cite that there were treatment-related adverse events including skin reactions in 66%, neuropathy occurred in 62%, and ocular disorders in 40%. And there was a little bit of pneumonitis in close to 9%, colitis, and hypothyroidism, so there are side effects to watch out for.  Dr. Neeraj Agarwal: So, Jeanny this is great. What is the key takeaway from this trial?  Dr. Jeanny Aragon-Ching: So I think the most important thing is we now have a new combination of EV and pembro which shows very promising responses and survival in part which led to the FDA accelerated approval in the cisplatin-ineligible population of patients. However, we must note that the phase 3 trial of EV302 will ultimately establish which approach is really beneficial for all of our cisplatin-ineligible patients, either a carboplatin-based chemotherapy regimen or a non-platinum-based regimen such as EV and pembro. Dr. Neeraj Agarwal: Thanks Jeanny, would you like to discuss any other study in the bladder cancer space? Dr. Jeanny Aragon-Ching: Absolutely. I think Abstract 4508 from Dr. Seth Lerner and colleagues will be very relevant to our colleagues. This abstract is SWOG S1011, which is a phase 3 surgical trial to evaluate the benefit of a standard versus an extended lymphadenectomy performed at the time of radical cystectomy for muscle-invasive bladder cancer.  Dr. Neeraj Agarwal: Yes. So this trial, as you said, is an important trial which randomized in a one-on-one fashion 618 patients with muscle-invasive bladder cancer undergoing radical cystectomy, and these patients were randomized to either standard lymph node dissection or an extended lymph node dissection. And standard lymph node dissection included, as we know, external and internal iliac and operative lymph node. The extended lymph node dissection included lymph nodes up to aortic bifurcation which included common iliac, presciatic, and presacral lymph nodes. At a median follow-up of approximately 6 years, there was no disease-free survival or overall survival benefit in patients undergoing an extended lymph node dissection compared to standard lymph node dissection. And extended lymph node dissection was also associated with greater morbidity and preoperative mortality. Dr. Jeanny Aragon-Ching: Very interesting data, Neeraj. So these results, I think, will be very useful for a lot of our surgical colleagues in both academia and the community who may still be inclined to perform extended lymphadenectomy during cystectomy. This study shows that it's actually not necessary. Dr. Neeraj Agarwal: Absolutely. So now let's move on to another disease type, which is very important - prostate cancer. There are several practice-informing abstracts that are worthwhile discussing. The first of these involves Abstract 5002, which looks at the impact of the PSA nadir as a prognostic factor after radiation therapy for localized prostate cancer, which will be presented by Dr. Praful Ravi and  colleagues. Jeannie, can you please tell us more about this abstract? Dr. Jeanny Aragon-Ching: Yeah, definitely. So this abstract, as you mentioned, Neeraj, is a prognostic impact of PSA nadir of more than or equal to 0.1 nanogram per ml within six months after completion of radiotherapy for localized prostate cancer - an individual patient data analysis of randomized trials from the ICECaP Collaborative. Basically, it refers to an attempt to evaluate early surrogate measures to predict for long term outcomes such as prostate cancer-specific survival, metastases-free survival, and overall survival. So they looked at a big registry from the ICECaP collaboration that included 10,415 patients across 16 randomized controlled trials. And those men underwent treatment for intermediate risk and high risk prostate cancer treated with either radiation therapy alone in about a quarter of patients, or they got RT with short-term ADT in about 58% of patients, and 17% of them got RT with long-term ADT.  So, after a median follow-up of ten years, what they found was, if you had a PSA nadir that is over or equal to 0.1 nanogram per ml within six months after completion of radiation therapy, it was associated with worse prostate cancer-specific survival, metastases-free survival, and overall survival. For instance, the five-year metastases-free survival for those who achieved a PSA nadir of less than 0.1 was 91% compared to those who did not, which was 79%. Therefore, they concluded that if you achieve a bad PSA of 0.1 or above within six months after you completed radiation, you had worse outcomes.  Dr. Neeraj Agarwal: Jeanny, what is the key takeaway message from this study? Dr. Jeanny Aragon-Ching: The key takeaway from this ICECaP analysis is that this information would be very important to augment a signal-seeking endpoint, especially for clinical trial development, so that we can develop further strategies to de-escalate for those who don't need systemic intensification or therapy intensification versus escalation for those who really do. Dr. Neeraj Agarwal: So, my radiation oncology colleagues need to watch out for those patients who do not achieve a PSA of less than 0.1 nanogram per ml within the first six months of finishing radiation therapy. Very interesting data.  Dr. Jeanny Aragon-Ching: Yes, absolutely. So. Neeraj another important abstract for our fellow clinicians, switching gears a little bit now, is Abstract 5011, which is titled “Do Bone Scans Overstage Disease Compared to PSMA PET?” This was an international, multicenter retrospective study with blinded, independent readers. Can you tell us more about this abstract? Dr. Neeraj Agarwal: Yes, a relatively small retrospective study, but still pertinent to our practice. So I'll summarize it. This study by Dr. Wolfgang Fendler and colleagues evaluated the ability of bone scans to detect osseous metastasis using PSMA PET scan as a reference standard. So in this multicenter retrospective study, 167 patients were included, of which 77 patients were at the initial staging of prostate cancer, 60 had biochemical recurrence after definitive therapy, and 30 patients had CRPC or castor-resistant disease.  These patients had been imaged with a bone scan and a PSMA PET scan within 100 days. And in all patients, the positive predictive value, negative predictive value and specificity for bone scan were evaluated at different time points. They had bone scan and PSMA PET scan and both were compared. And what they found was interesting. All these three values - positive predictive value, negative predictive value, and specificity for bone scan were 0.73, 0.82 and 0.82 in all patients, and in initial staging, it was even lower at 0.43 and 0.94 and 0.80.  So, without getting into too much detail regarding these numbers, I want to highlight the most important part of the study, that at the initial staging, 57% patients who had a positive bone scan had false positive bone scans. The interreader agreement for bone disease was actually moderate for bone scans and quite substantial for the PSMA PET scan.  Dr. Jeanny Aragon-Ching: So, Neeraj, what do you think is the key takeaway message here for our audience?   Dr. Neeraj Agarwal: The key takeaway message is that positive predictive value of bone scan was low in prostate cancer patients at initial staging, with the majority of positive bone scans being false positive. This suggests that a large proportion of patients which we consider to have low-volume metastatic disease by bone scan actually have localized disease. So in the newly diagnosed patients with prostate cancer, patients should ideally have a PSMA PET scan to rule out metastatic disease.   So, let's move on to another abstract I would like to discuss, which has important implications in treatment, especially now that lutetium 177 is approved, but frankly not available widely. Dr. Jeanny Aragon-Ching: Yeah, that's actually very timely. So the abstract you're referring to is 5045, which is being presented by Dr. Yu Yang Sun and colleagues entitled “Effects of Lutetium PSMA 617 on Overall Survival in TheraP Versus VISION Randomized Trials: An Exploratory Analysis.” So, Neeraj, can you tell us more about the relevance of this exploratory analysis? Dr. Neeraj Agarwal: Definitely. In this abstract, Dr. Yang Sun and colleagues assess the effect of lutetium PSMA on overall survival in two different trials, TheraP and VISION trials. So, just for our listeners' recollection, the phase 2 TheraP trial compared lutetium PSMA and cabazitaxel in patients with mCRPC who had progression on docetaxel and had significant PSMA avidity on gallium PSMA pet scan, which was defined as a minimum uptake of SUV max of 20 at least one site of disease and SUV max of more than 10 at all sites of measurable disease.  In this trial, 20 of 101 patients in the cabazitaxel arm crossed over to lutetium PSMA, and 32 of 99 patients in the lutetium PSMA arm crossed over to cabazitaxel. In the VISION trial, patients with mCRPC who previously progressed on at least one ARPI and one taxane-based therapy and had a positive gallium PSMA scan, and here, positivity was not stringently pre-specified as it was done in the context of TheraP trial. So, positive gallium pet scans were randomly assigned in two to one fashion to receive either lutetium PSMA plus best supportive care or standard of care versus standard of care.  And I'd like to highlight that the standard of care comprised ARPIs and bone protecting agents and these patients were not allowed to have cytotoxic chemotherapy such as cabazitaxel in the standard of care arm. Now, overall survival was similar in the lutetium PSMA group regardless of whether they got lutetium PSMA in the VISION trial or TheraP trial. There was no difference in overall survival with lutetium in the lutetium arms of VISION and TheraP trial with a hazard ratio of 0.92. And there was no difference in the overall survival between the lutetium PSMA and the cabazitaxel group in the TheraP trial if you use counterfactual analysis, assuming crossover had not occurred. So, quite interesting in my view. Dr. Jeanny Aragon-Ching: Yeah, thanks Neeraj for that wonderful synopsis and discussion. So, what is the key take home message then? Dr. Neeraj Agarwal: The main message in this new exploratory analysis, which combined both the TheraP and VISION trials, is that lutetium PSMA and cabazitaxel seem to be associated with similar overall survival benefit in these highly selected patients with PSMA positivity. Additionally, the difference in the observed effect of lutetium PSMA and overall survival in the TheraP and VISION trials may be actually better explained by the use of different treatments in the respective control arms of these trials. And these results, in my view, are quite pertinent for those patients and providers who do not have access to lutetium-177 therapy.  Let's go to another abstract that is currently relevant to our practice, given many patients with advanced prostate cancer who have concurrent diabetes; I'm talking about Abstract 5066. Jeanny, can you please tell us more about this abstract?  Dr. Jeanny Aragon-Ching: Certainly, Neeraj. So this abstract will be presented by Dr. Amy Shaver and colleagues. So it's also very relevant, since many men who are diagnosed with prostate cancer frequently also have a concomitant diagnosis of type 2 diabetes mellitus. So, this was a SEER-Medicare population database analysis that looked at men who were treated with either abiraterone or enzalutamide and also had concomitant diagnosis of type 2 diabetes mellitus (DM). And they were identified using ICD-9 and ICD-10 codes and they were all tied in to acute care utilization. So they looked at CMS research data codes and ER hospitalization visits six months after treatment initiation was recorded. So all in all, they took a sample of 11,163 men, of whom close to 62% were treated with abiraterone and about 38% were treated with enzalutamide.  So, of these, about 27% of them had type 2 DM, of whom 59% received abiraterone and about 41% had enzalutamide. So, the bottom line is, compared to those without diabetes mellitus, those who had type 2 diabetes had worse acute care utilization, which was 43% higher than those who got abiraterone compared to enzalutamide, and also had higher overall mortality. Therefore, the bottom line is, having type 2 diabetes mellitus, unfortunately, portends worse outcomes in men with prostate cancer, so careful attention needs to be paid to those who are starting out already with such comorbidities. So Neeraj, any final thoughts you have regarding this abstract and overall before we wrap up on the podcast today?  Dr. Neeraj Agarwal: Absolutely. So it looks like, based on this very important pertinent Abstract 5066, which talks about the impact of diabetes on our patients, I think we need to be very watchful regarding the impact of diabetes on our patients who are being treated with abiraterone or enzalutamide, especially drugs which are known to make the metabolic syndrome and diabetes worse. I think close monitoring and close attention to control of diabetes is very important. So with that, I would urge the listeners to come and join us at the Annual Meeting, not only to celebrate these successes but also to help disseminate this cutting-edge data to practitioners and maximize the benefit to our patients across the globe.   And thank you to our listeners for joining us today. You will find links to the abstracts we discussed today on the transcript of this episode. Finally, if you value the insights that you hear on our ASCO Daily News Podcast, please take a moment to rate, review and subscribe wherever you get your podcast.  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. Neeraj Agarwal @neerajaiims Dr. Jeanny Aragon-Ching Follow ASCO on social media:   @ASCO on Twitter   ASCO on Facebook   ASCO on LinkedIn     Disclosures:  Dr. Neeraj Agarwal:   Consulting or Advisory Role: Pfizer, Bristol-Myers Squibb, AstraZeneca, Nektar, Lilly, Bayer, Pharmacyclics, Foundation Medicine, Astellas Pharma, Lilly, Exelixis, AstraZeneca, Pfizer, Merck, Novartis, Eisai, Seattle Genetics, EMD Serono, Janssen Oncology, AVEO, Calithera Biosciences, MEI Pharma, Genentech, Astellas Pharma, Foundation Medicine, and Gilead Sciences  Research Funding (Institution): Bayer, Bristol-Myers Squibb, Takeda, Pfizer, Exelixis, Amgen, AstraZeneca, Calithera Biosciences, Celldex, Eisai, Genentech, Immunomedics, Janssen, Merck, Lilly, Nektar, ORIC Pharmaceuticals, Crispr Therapeutics, Arvinas  Dr. Jeanny Aragon-Ching: Honoraria: Bristol-Myers Squibb, EMD Serono, Astellas Scientific and Medical Affairs Inc., Pfizer/EMD Serono Consulting or Advisory Role: Algeta/Bayer, Dendreon, AstraZeneca, Janssen Biotech, Sanofi, EMD Serono, MedImmune, Bayer, Merck, Seattle Genetics, Pfizer, Immunomedics, Amgen, AVEO, Pfizer/Myovant,  Exelixis, Speakers' Bureau: Astellas Pharma, Janssen-Ortho, Bristol-Myers Squibb, Astellas/Seattle Genetics.

In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Jenny Mueller and Bill Zammarrelli to discuss molecular classification and risk stratification in endometrial cancer. Jenny Mueller, MD, is a gynecologic oncologist and assistant attending in the department of surgery at Memorial Sloan Kettering Cancer Center. She leads the endometrial cancer research team at MSKCC with an emphasis on prospective, translational, and collaborative efforts within and across institutions. Bill Zammarrelli, MD, currently works as a gynecologic oncology fellow at Memorial Sloan Kettering Cancer Center. He is a commissioned officer in the US Army and completed his residency at Walter Reed National Military Medical Center. His current research focuses on the genetics of endometrial cancer. Highlights: - PORTEC-1 and GOG-99 risk classifications are discordant for stage I grade 3 endometrioid endometrial carcinoma (EEC). - Stage I grade 3 EECs of CN-high molecular subtype have a worse 3-year progression-free survival compared to non-CN-high molecular subtypes. - Molecular classification in combination with clinicopathologic factors may provide improved prognostic information.

Welcome to The Herd FIT Podcast @herdfitpodcast with Coaches David Syvertsen @davesy85 and Sam Rhee @bergencosmetic. This podcast is aimed at helping anyone and everyone looking to enhance their healthy lifestyle through fitness, nutrition, and most importantly, MINDSET.Dave and Sam welcome someone who truly has achieved amazing success in every endeavor. Special guest Dr. Allison Warner, MD PhD, is not only an oncologist specializing in melanoma at Memorial Sloan Kettering Cancer Center (soon to be at Stanford University Medical Center), but she has been involved with CrossFit at every level since 2009, as a CrossFit Games athlete, a CF L-1 certified coach, and part of the CrossFit Health @crossfithealth initiative. She also is a dedicated athlete at our own @crossfitbison, who will be sorry (but proud!) to see her going to the West Coast soon.Allison talks with Dave and Sam about her CrossFit experience through her medical training, why she has continued with CrossFit all these years, and important takeways for anyone interested in health and fitness.Dr. Warner obtained her undergraduate degree at Cornell University where she was a varsity gymnast. She graduated from Duke University with her MD/PhD degrees and subsequently completed a residency in internal medicine at Massachusetts General Hospital. After a fellowship in oncology at Memorial Sloan Kettering Cancer Center (MSKCC), she has been an assistant attending physician at MSKCC. She will be taking a position at Stanford University Medical Center next month.@crossfittraining @crossfit @crossfitgames #crossfit #sports #exercise #health #movement #crossfitcoach #agoq #clean #fitness #ItAllStartsHere #CrossFitOpen #CrossFit #CrossFitCommunity @CrossFitAffiliates #supportyourlocalbox #crossfitaffiliate #personalizedfitness 

Cancer is widespread in humans around the world, and with that, there are many myths, misconceptions, and fears attached to it. But it can be treated, healed, and prevented. There was a time in the medical community when the goal of treating was mere survival. But times have changed, technology and research has advanced and medical professionals now have more awareness about increasing survival and QOL.  The answer to this lies in - INTEGRATIVE ONCOLOGY.    In this episode of Healing Cancer The Right Way, host Samara Mahindra (Founder of CARER- India's first Integrative Oncology Platform) discusses with the Father of Integrative Oncology - Dr. Gary Deng about how Integrative Oncology directly impacts a patient's healing.  Dr. Deng is a Medical Director of the Bendheim Integrative Medicine Center at Memorial Sloan Kettering Cancer Center (MSKCC) and Professor of Clinical Medicine at Weill Cornell Medical College of Cornell University in New York. His professional expertise is in the use of an integrative medicine approach to help patients throughout the continuum of cancer prevention, treatment, and survivorship. Dr. Deng has taken a leadership role in the emerging and evolving field of integrative oncology. He has built a robust integrative medicine physician practice and directs clinical services provided at the At Bendheim Integrative Medicine Center at MSKCC.  Dr. Deng is actively conducting some incredible research and developing innovations in the field. Listen as they talk about: What exactly is Integrative Oncology and what kind of developments have taken place. - A brief intro to immunotherapy- Importance of Diet and working on balancing your immunity- Indian Food Diet v/s Western Food Diet- Herbs and medicines that can help you heal better & lots more   You can follow us and leave us feedback on Facebook, Instagram, and Twitter @eplogmedia, or send us an email at bonjour@eplog.media DISCLAIMER: Please note that the points discussed in this podcast should not be relied upon as conclusive medical advise in any manner.The views expressed on all the shows produced and distributed by Ep.Log Media are personal to the host and the guest of the shows respectively and with no intention to harm the sentiments of any individual/organization.The said content is not obscene or blasphemous or defamatory of any event and/or person deceased or alive or in contempt of court or breach of contract or breach of privilege, or in violation of any provisions of the statute, nor hurt the sentiments of any religious groups/ person/government/non-government authorities and/or breach or be against any declared public policy of any nation or state.  See omnystudio.com/listener for privacy information.

In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez is joined by Drs. Mario Leitao and Evan Smith to discuss outcomes of low-grade endometrial stromal sarcoma. Dr. Leitao is an attending surgeon and member at Memorial Sloan Kettering Cancer Center as well as a Professor at Weill Cornell Medical College. He serves as the fellowship director at MSKCC as well as the Director of the Minimally Invasive and Robotic Surgery Program. Dr. Smith is a gynecologic oncologist at Woman's Hospital in Baton Rouge, Louisiana. He also serves as an Assistant Clinical Professor of Gynecologic Oncology with the LSU Health Obstetrics and Gynecology residency program in Baton Rouge. Highlights: -Lymphadenectomy is unnecessary in patients with low-grade endometrial stromal sarcoma (ESS) and clinically normal nodes. -Postoperative therapies do not improve progression-free survival (PFS) or overall survival in low-grade ESS that is completely resected. -FIGO stage is associated with PFS but not disease-specific survival. -Next generation sequencing is standard for soft tissue sarcomas and should be offered to patients with low-grade ESS.

For episode 19 of the Ori Spotlight Podcast, Jason C. Foster is joined by Isabelle Rivière, Director of Cell Therapy and Cell Engineering Laboratory at the Memorial Sloan-Kettering Cancer Center (MSKCC), one of the world's leading cancer centers. Isabelle has also recently joined Ori as our newest SAB member – we're honored to have her supporting us in achieving our mission. To this episode, Isabelle brings insights she has gathered from 25 years of experience within the cell and gene therapy industry. Isabelle is also a co-founder of Juno Therapeutics, a board member of the American Society of Gene and Cell Therapy (ASGCT), and past board member of the Alliance for Regenerative Medicine (ARM). Together, Jason and Isabelle explore the most significant barriers to treating patients at scale, how automated systems - to improve monitoring, recording and tracking could help make therapies more affordable, and the importance of industry partnerships to accelerate the development of therapies and implementation of new technologies. Learn more about Isabelle Rivière

In this week's episode featuring Thalyana Stathis, Ph.D., Manager, Office of Career & Professional Development, Memorial Sloan Kettering Cancer Center, we discuss an array of topics related to career advancement and effective communication for scientists, including: - How Thalyana's involvement in ballet and Greek dance during her undergraduate studies at Cornell and also while earning her Ph.D. at Yale provided space for her to gain perspective and relieve stress during her Ph.D. program. - Thalyana's extensive involvement in Toastmasters in New York City, including what motivated her to join, how Toastmasters helped her sharpen communication skills, and why she encourages researchers at Memorial Sloan Kettering Cancer Center to participate in Toastmasters. - Principles Thalyana advises MSKCC researchers to apply in their own editing and presentation process that could also aid listeners. - Details about Thalyana's career transitions, networking, and helpful lessons she learned along the way. - Thalyana's current role at MSKCC and the work she and her colleagues do to assist researchers with science communication. Resources mentined in the espisode Thalyana Stathis, Ph.D. Toastmasters' New York City chapter Alan Alda Center for Communicating Science New York Academy of Sciences

Dr. Anthony Rossi is well known as a board-certified dermatologist recognized internationally as a leading expert on sensitive skin. Dr. Rossi serves as the dermatologist and laser expert at the prestigious Memorial Sloan Kettering Cancer Center in NYC where he specializes in dermatologic surgeries for the treatment of skin cancers and benign skin conditions that arise during and after cancer therapy. In addition to his exceptional work at MSKCC, Dr Rossi has spent 10+ years applying his research to develop his own line of innovative skincare products that utilize his breakthrough Bio-Theriac Complex™. The proprietary system targets the skin's TRVP1 receptors which have been scientifically proven to directly correlate to premature skin aging when there is over-activity present. Tune in to our exclusive interview with the Scientific Genius himself as he walks us through why the science and technology of this innovative approach to skin health is designed for everyone and is serving the needs of thousands who suffer from normal to problematic skin concerns. --- Send in a voice message: https://anchor.fm/skincareanarchy/message Support this podcast: https://anchor.fm/skincareanarchy/support

പ്രിയ സുഹൃത്തേ , ന്യൂയോർക്കിലെ പ്രശസ്തമായ Memorial Sloan Kettering Cancer Center (MSKCC ) അർബുദത്തിന് ഫലപ്രദമായ ഒരു മരുന്ന് വികസിപ്പിച്ചു എന്ന വാർത്ത ലോകത്തെ തെല്ലൊന്നുമല്ല ആശ്വസിപ്പിച്ചത് . MSKCC യിൽ അസ്സോസിയേറ്റ് പ്രൊഫസറായ മലയാളി ഡോക്ടർ വിജയ് ജോസഫ് പുതിയ കണ്ടെത്തലിൻ്റെ വിശദാംശങ്ങൾ പങ്കുവെയ്ക്കുന്നു ഈ പ്രത്യേക അഭിമുഖത്തിൽ . അദ്ദേഹം പ്രധാനമായും സംസാരിക്കുന്നത് ഇനിപ്പറയുന്ന വിഷയങ്ങളെക്കുറിച്ചാണ് . 1 . എന്താണ് Dostarlimab എന്ന പുതിയ മരുന്ന് മുന്നോട്ടുവെയ്ക്കുന്ന പ്രതിവിധി ? എത്രമാത്രം വിജയപ്രതീക്ഷ ഇതുനൽകുന്നു ? 2 . ഏതുതരം അർബുദങ്ങൾക്കാണ് പുതിയ മരുന്ന് ഫലപ്രദമാകാൻ ഇടയുള്ളത് ? 3 . എന്താണ് അർബുദചികിത്സാരംഗത്ത് Immunotherapy യിൽ നടക്കുന്ന പരീക്ഷണങ്ങൾ ? 4 . പുതിയ മരുന്നിനെക്കുറിച്ച് ഉയരുന്ന സംശയങ്ങൾ എന്തൊക്കെയാണ് ? 5 . അർബുദമരുന്നുകൾക്ക് തീപിടിച്ച വില എന്തുകൊണ്ട് ? ആരോഗ്യനയം എങ്ങനെ പരിഷ്കരിക്കപ്പെടണം ? 6 . പുതിയ മരുന്ന് വിജയമാണെങ്കിൽ മരുന്ന് ലോകത്ത് ലഭ്യമാകാൻ എത്രസമയമെടുക്കും ? തിരുവനന്തപുരം Sree Chitra Tirunal Institute for Medical Sciences & Technology ൽ നിന്നും PhD കരസ്ഥമാക്കിയ ഡോക്ടർ വിജയ് ജോസഫ് പന്ത്രണ്ടുകൊല്ലങ്ങളായി Memorial Sloan Kettering Cancer Center (MSKCC ) ലാണ് . പോഡ്‌കാസ്റ്റിലേക്ക് സ്വാഗതം . സ്നേഹപൂർവ്വം എസ് . ഗോപാലകൃഷ്ണൻ 11 ജൂൺ 2022 ഡൽഹി https://www.dillidalipodcast.com/

Dr. Joe Sirintrapun is a surgical pathologist and genitourinary tumor expert, currently serving as the Director of Pathology Informatics at MSKCC. Joe joins Beyond the Scope to discuss his journey to the current role at MSKCC, revealing the value of overcoming setbacks and defining some of the qualities needed to be a leader in the field of Informatics. Previously the President of The Association for Pathology Informatics (API), Joe talks about all of the work that was involved in the CLIA relaxation of regulation for remote sign-out and gives a status update about how long this may last. The 2022 API Summit is being held May 9-12 in Pittsburgh, PA. Please click here for more information.

Tara Notrica is 57 years old and a mother to 2 children, Jared, age 21 and Samantha, aged 17. She's been married to Barry for 24 years and they live in New York Prior to becoming ill with a rare disease called Mast Cell Disease, she was a Special Education Teacher/Administrator. Her disease causes her to have anaphylactic episodes from multiple triggers, which can cause anaphylactic shock Since there is no cure and very few medications for her disease, her transplant doctor and Tara decided to proceed with having a transplant.  In July 2015, she had an autologous stem cell transplant using her own stem cells. In June 2018, she had an allogeneic bone marrow transplant from an unrelated donor.  However, due to various complications, she was hospitalized extensively at MSKCC in New York City.  Her story has been made into a documentary called “Second Chance” featuring all original music co-written and recorded by Samantha The full documentary will be available to the public in Spring 2022, after it has finished completing the film festival circuit Some key points from our interview:·        How despite feeling that her body is semi broken, she feels that her spirit, courage, and resilience remains unbroken·        How whatever is going on with her health she always tries to persevere·        How it took five years before she would receive her diagnosis·        How her resilience developed by her determination to be here for her children and desire to watch them grow up·        How despite her many health conditions she still finds time to lobby for changes in the law to offer transport to children whose parents are unable to take them to school due to ill health·        How she's determined to raise awareness about rare diseases and stem cell transplants·        How her daughter Samantha has recorded nine separate songs for the documentary “Second Chance” which reflects all the different topics they went through as a family   https://www.instagram.com/taranotrica/Instagram-TaraNotrica Trailer Link/Film Information www.4thcoastproductions.com/secondchancedocumentary "Unbroken: Healing Through Storytelling" features  individuals who have all triumphed after adversity and have not just bounced back in life, but forward and are now making a difference for others.Hosted by Madeleine Black, the show will share stories of all the amazing people Madeleine has met on her own journey as an author/speaker and these stories will heal, motivate, inspire and bring hope when they share their wisdom and knowledge with her.She really believes in the power that comes when we share our stories, that in fact we are not story tellers but story healers. Tune in to discover what helped them to stay unbroken and together we will discover that none of us are broken beyond repair.You can find out more about Madeleine, her story and her memoir, Unbroken,  from her website: https://madeleineblack.co.ukWatch the edit on You Tube as well! https://youtu.be/-NfVe_jb0ag   

Hi friends, this is Dr. Michael Williams and welcome to another episode of the diversify in path podcast. This podcast explores how investing in diversity can lead to a high return of investment in pathology and laboratory medicine by learning from the knowledge and experiences of diverse voices within in our field.  My next guest is Dr. S. Joseph SirintrapunDr. Sirintrapun is the Director of Pathology Informatics at Memorial Sloan Kettering Cancer Center (MSKCC) and an Associate Attending and member of the Warren Alpert Center for Computational Pathology at MSKCC. Dr. Sirintrapun is board certified in Anatomic and Clinical Pathology and Clinical Informatics. In addition to his work in informatics, he practices surgical pathology specializing in genitourinary tumors.Dr. Sirintrapun is the current 2021 President of the Association for Pathology Informatics (API). His primary efforts are in data and systems engineering and leadership, as it relates to digital and computational pathology. He works towards a better understanding of the cognitive and social impacts of technology on clinical practice, and particularly on operationalization or the translation of innovations in digital pathology and computational pathology to practice. Dr. Sirintrapun is also passionately engaged in cultivating a diverse, equitable, and inclusive younger medical and technological workforce to propel pathology informatics and computational pathology into the future.Linked-In:  S. Joseph Sirintrapun | LinkedIn

David Klimstra is the Chief Medical Officer at Paige and was previously the Chair of Pathology at Memorial Sloan Kettering Cancer Center. Paige is a medical company offering the first FDA cleared artificial intelligence platform to assist with the diagnosis of prostate cancer. Dr. Klimstra joins the show to discuss building a robust digital pathology program at MSKCC and the transition from academia to industry. Furthermore, he offers insights into what the first FDA clearance for an AI product means to the industry and the overall breadth of AI applications in pathology.

In this episode of the IJGC podcast, Editor-in-Chief Dr. Pedro Ramirez, is joined by Dr. Mario Leitao to discuss prophylactic negative pressure wound therapy RCT. Dr. Leitao is currently an Attending Surgeon in the Department of Surgery at Memorial Sloan Kettering Cancer Center and a Professor in the Department of Obstetrics and Gynecology at Weill Cornell Medical College. He currently serves as Program Director for the Gynecologic Oncology Fellowship. Dr. Leitao is also the Director for the Minimal Access and Robotic Surgery Program in the Department of Surgery for MSKCC. Dr. Mario Leitao is currently an Attending Surgeon in the Department of Surgery at Memorial Sloan Kettering Cancer Center and a Professor in the Department of Obstetrics and Gynecology at Weill Cornell Medical College. He currently serves as Program Director for the Gynecologic Oncology Fellowship. Dr. Leitao is also the Director for the Minimal Access and Robotic Surgery Program in the Department of Surgery for MSKCC. Highlights 1. SSI is a common postoperative complication that leads to significant healthcare costs in the near- and far-term 2. In our RCT, the use of a negative pressure wound therapy (NPWT) system did not improve wound complications (Superficial SSI) in a cohort of patients undergoing mostly laparotomy for gynecologic malignancies with closed laparotomy incisions. 3. There was also no signal of benefit in the small subgroup of morbidly obese patients. 4. Increasing BMI was the only independently associated risk for the development of a wound complication @leitaomd @sloan_kettering

Trained in nursing Dr. Coyle began her palliative care career in pain control at MSKCC. She has mentored and educated nurses internationally as well as written books, and numerous, chapters, and articles. She was co-editor of the early editions of the Oxford Textbook of Palliative Nursing. She has lectured extensively on pain and palliative care as well as ethical issues for nurses and was a consultant for the New York State Task Force on Life and the Law, Committee on Assisted Suicide and Euthanasia.

Dr. Jeanine Cook-Garard learns more about gynecological cancers and their surgical options with Dr. Jennifer Mueller, a surgeon who specializes in caring for women with gynecological cancers at Memorial Sloan Kettering Cancer Center.

Dr. Nirupa Raghunathan is a Med/Peds physician, and the director of Pediatric Integrative Medicine at MSKCC. She has a background in pediatrics and adult medicine, which allows her to follow patients from adolescence to young adulthood. We discuss the role of integrative oncology in pediatrics, modalities that can be used, specific issues that AYA patients have, and how it can be advanced worldwide.

Raj and Matt join Beyond the Scope to discuss the the Digital Anatomic Pathology Academy, hosted on PathPresenter - a primarily open source cloud based viewing platform for digital slides. DAPA is used as an educational, clinical, and publication tool. DPA members can access DAPA for free to make use of the numerous educational modules (dpa-dapa.com).NOTE: this episode utilizes video for platform tutorials. Please visit https://digitalpathologyassociation.org/dpa-podcast-beyond-the-scope for the video version.2:48 Guest intro7:21 Introduction to the cloud based viewing and educational platform8:47 Tutorial for navigating the platform17:20 DAPA educational module features and demonstration20:45 DAPA use cases; including an interactive way to study for boards26:00 How DPA members and other can access the platform27:50 Open source platform vs. licensed version for private data30:10 MSKCC experience using the platform as an education portal and conference tool33:00 Long term clinical goals of the platform37:55 Utilizing the platform in underserved areas39:23 Utilizing the platform for publications and E-books

In this episode, Carol L. Brown, MD, discusses her role as chief health equity officer at MSKCC, her thoughts on the future of structural inequities, strategies to diversify clinical trials, and more. Welcome to another exciting episode of Oncology Overdrive :13 About Brown :19 The interview 3:00 Can you tell us a little bit about your path? 3:10 Are equity officer positions helping institutions, or are they there as window dressing? 6:46 Are you optimistic with where we're going? Do you think we'll come out of the pandemic with new solutions to break down these structural inequities? 11:35 We must keep focusing on these issues 18:04 How does fear play a role in how we speak with and care for our patients? 21:22 Do you have ideas on how we can get more heterogenous populations in clinical trials? 33:00 Brown's take-home message 40:09 How to reach Dr. Brown 41:11 Carol Brown, MD, is a board-certified gynecologic oncologist; senior vice president and chief health equity officer at Memorial Sloan Kettering Cancer Center and the incumbent of the Nicholls-Biondi Chair for Health Equity. She also serves as vice chair of Health Equity in the department of surgery. She holds academic appointments as attending surgeon and member at MSK, and professor, obstetrics and gynecology at Weill Cornell Medical College. We'd love to hear from you! Send your comments/questions to Dr. Jain at oncologyoverdrive@healio.com. Follow us on Twitter @HemOncToday and @ShikhaJainMD. Brown can be reached by email at healthequity@mskcc.org. Disclosures: Brown reports no relevant financial disclosures. Jain reports she is a paid freelance writer for Lippincott.

Hosts Jack West and Charu Aggarwal meet with Dr. Vince Miller to discuss the process of deciding to move from academia to industry, the evolution of molecular marker testing, and the potential for EQRx to break the impasse of escalating cancer drug costs.

Dr. Britta Weigelt of MSKCC discusses her team's study on synchronous endometrial (EC) and ovarian carcinomas (OC) in Lynch syndrome and constitutional Mismatch Repair Deficiency Syndrome (CMMRD). Contrary to sporadic synchronous ECs/OCs, which are almost invariably clonally related, ECs/OCs simultaneously involving the uterus and ovary in LS patients may represent two independent primary tumors. Like their sporadic counterparts, a subset of MMR deficiency syndrome-related synchronous ECs/OCs may also originate from a single with the endometrium being the likeliest site of origin.Study by Weigelt et al, Clonal relationship and directionality of progression of synchronous endometrial and ovarian carcinomas in patients with DNA mismatch repair-deficiency associated syndromes. Modern Pathology, 34, 994-1007, 2021. https://www.nature.com/articles/s41379-020-00721-6. See acast.com/privacy for privacy and opt-out information.

In this episode of Smart Energy Voices, host Debra Chanil discusses several innovative retro-commission projects with Robert Berninger, Director of Plant Operations, Energy and Engineering at Memorial Sloan Kettering Cancer Center (MSKCC). Bob oversees more than 4 million square feet of critical care facilities in the heart of New York City. Listen as he recounts his experience evaluating potential projects so you can benefit from the great insights Bob has to share. You will want to hear this episode if you are interested in... Robert Berninger's role at MSKCC [02:18] Sloan's innovation award [03:28] The importance of FDD (Fault Detection & Diagnostics) [05:24] Current retro-commissioning [09:44] Cogeneration projects [11:11] Sloan Kettering's vendor vetting process [14:49] Beginning Moves to Fault Detection & Diagnostics Robert Berninger oversees approximately eleven buildings as well as the entire energy budget for the institution. Bob started at MSKCC as the Energy Manager and has worked with them for over fifteen years. In his time there, the institution has kept its energy footprint steady while also doubling in square footage. A significant factor in that achievement was Fault Detection & Diagnostics (FDD). Bob was initially leery of fault detection. He thought it would highlight issues in the building that they couldn't correct due to other issues. They began with a systematic approach, starting with the chilled water plant, heating plant, and ended with the VAV box level. With FDD, MSKCC is alerted when an issue occurs rather than waiting for a problem to be reported. This reduction in time from issue to resolution has saved energy, time, and money. Innovation Awards In 2020, MSKCC won the Smart Energy Decisions Innovation Award for Healthcare Energy Data Management for Virtual Energy Monitoring and Fault Detection and Diagnostics. The project started as a response to New York City Local Law #87, which requires all buildings over 25,000 square feet to have an energy audit and retro-commissioning every ten years. In 2018, the Breast and Imaging Center at MSKCC was due for this audit, so they engaged a vendor to create a report. MSKCC used this report to come up with several capital ECMs (energy conservation measures) that had been highlighted. One of the projects was to install a virtual energy managing and fault diagnostic system. This addition was in response to the finding that any time a system was retro-commissioned, the energy usage would gradually increase and undo the initial benefits if the system wasn't constantly monitored. With fault detection and diagnostics, MSKCC is able to find out immediately if something wasn't working correctly. This warning allows them to address issues and maintain the benefits of the original adjustments. The Positive Results of Retro-commissioning Bob defines retro-commissioning as bringing the building back to its original design intent. Recommissioning is going back and commissioning the building again if the building was commissioned in its beginning. And finally, continuous commissioning is using the tools that you have with the BMS and FDD to make sure that the building is operating at its design intent at all times. The continuous detection will provide an alert if something within the system drifts, allowing an immediate repair.  The main campus of MSKCC is using steam to hot water conversion along with cogeneration. The three buildings in the project use Con Ed steam, which is a relatively wasteful system. MSKCC is working on converting 130 air handlers using steam preheats to hot water, changing out the coils, or re-using their chilled water coils for heating using low-temperature hot water. They're also installing a total of 3.3 MW of cogeneration, which is matched to their base heating load so that there's no waste of heat. Overall the project will save the institution about $8-10 million per year in energy costs. That's an improvement anyone can support. Resources & People Mentioned 2020 Innovation Awards Local Law #87 Local Law #97 Connect with Robert Berninger On LinkedIn Robert (Bob) Berninger is the Director of Plant Operations, Energy and Engineering at Memorial Sloan Kettering Cancer Center (MSKCC). In his 15 years with MSKCC, Bob has held various positions, first as the Energy Manager, overseeing and implementing energy conservation projects, and then as Plant Operations Manager. Currently, he is a Director managing the day-to-day operations of the HVAC systems and staff, overseeing the energy management systems and energy budgets, exploring and implementing energy conservation measures. Prior to this position, Bob was the Assistant Manager of the Physical Plant at Columbia University. He holds a B.E. in Marine Engineering from SUNY Maritime College. Robert is a Certified Energy Manager (CEM), Certified Energy Auditor (CEA), and a Certified Sustainable Development Professional (CDSP). He also holds a United States Coast Guard Chief Engineer's Steam and First Engineer Motor License. He is a member of the Association of Energy Engineers and is a past President of the New York City Chapter of AEE. Bob was awarded the International Energy Manager of the Year in 2016 by the Association of Energy Engineers. Connect With Smart Energy Decisions https://smartenergydecisions.com Follow them on Facebook Follow them on Twitter Follow them on LinkedIn Subscribe to Smart Energy Voices If you're interested in participating in the next Smart Energy Decision Event, visit smartenergydecisions.com or email our Event Operations Director, Lisa Carroll at lisa@smartenergydecisions.com Audio Production and Show notes by PODCAST FAST TRACK https://www.podcastfasttrack.com

Hosts Jack West and Charu Aggarwal discuss with Dr. Samyukta Mullangi of Memorial Sloan-Kettering the limitations of the current state-based medical licensing requirements and several potential paths to adapt to telemedicine & current practice needs.

Ralph W. Moss, Ph.D Cancer, Incorporated Cancer, Incorporated is a blistering critique of the greed and lies of the cancer drug business, and shows how Big Pharma’s deceptions have caused suffering and cost lives! This book reveals Big Pharma’s manipulation of every aspect of cancer drug development. This has resulted in a host of minimally effective, unsafe and outrageously priced drugs. Since the mid-1970s, Ralph W. Moss, PhD, has been writing about alternative and complementary cancer treatments. His journalistic efforts began as a science writer for Memorial Sloan-Kettering Cancer Center in New York City. He also began “Second Opinion,” an underground newsletter that shed light on drug industry influence over his employer, MSKCC. After being fired by MSKCC as a whistle-blower in 1977, Moss wrote The Cancer Industry (1980). This was a full-scale exposé of President Nixon’s “War on Cancer.” This book, published by Grove Press and featured on CBS’s 60 Minutes, took a deep look at the confluence of money and medicine in the cancer field. In the 1990s, Moss was a founding advisor of the NIH ‘s influential Office of Alternative Medicine (now the $151.9 million National Center for Complementary and Innovative Health). After writing Questioning Chemotherapy in 1996, Moss continued to write books, articles, scientific papers, and blog posts on the topic, including Customized Cancer Treatment, Antioxidants Against Cancer, and Doctored Results (2015), which coincided with Eric Merola’s documentary, Second Opinion. In both of these, Moss considered the fierce laetrile controversy of the 1970s from a 21st Century perspective. Along with his recent book-length exposé, Cancer, Incorporated, and a leading role in his grandson Jacob Moss’s hour-long film, Immunotherapy: The Battle Within, The Moss Report podcast is Dr. Moss’ latest effort to move the field of oncology in a more natural, humane, and non-toxic direction. Show highlights: Ralph W. Moss has written ten books and made three documentaries about cancer, including Cancer Incorporated. His alternative research started when he was fired from Sloan Kettering Cancer Center. How effective is Laetrile for cancer? Who is Dr. Paul Gerhardt Seeger? Why is Ralph W. Moss “the world’s worst party guest”? Is there a “magic bullet” for cancer? “First do no harm” doesn’t mean no harm is possible at all. “Start with the least damaging treatment, and then work your way up if you have to,” according to Ralph Moss. Does chemotherapy have any value? What is exclusion criteria? Inclusion criteria? Why do wealthier and healthier people have a better chance at beating cancer? How does this influence cancer research? His latest book, Cancer, Incorporated, is available for free. It exposes the Dark Side of Big Pharma. The corruption is far-reaching. “I believe it will blow the socks off most of your audience,” he asserts. “There are so many ways you can take a study and spin it.” What is personalized cancer medicine? What’s wrong with Big Pharma wanting to make a drug for every mutation? What replaced the environmental cancer research of the 1980s? Why did molecular biologist James Watson say the genetic approach to cancer is never going to work? What percent of cancer cases are actually caused by genetics? What about the metabolic nature of cancer? Where did cancer originate? Did our ancestors have as much cancer as we do? These are questions today’s cancer researchers aren’t comfortable with. How long did our ancestors live? What did they eat? Broccoli is a poison for worms and caterpillars, but a cancer therapy for human beings. Is cooked broccoli as good as raw?

You know back in the olden days when a foot of measurement was actually the measure of your own foot? So, I might measure something and it’s, like, 19 feet. And then you measure the same exact thing and it’s 38 feet because you have tiny feet. This is the analogy that kept running through my mind as I was talking with Anna Kaltenboeck in this health care podcast about QALYs to measure the value of drugs. In this metaphor, QALYs are the ruler so that 1 foot of drug value is the same for everybody and all drugs. It’s very civilized as a concept if you think about it. QALY stands for quality-adjusted life year. The goal of a QALY is to figure out how much any given drug is worth to a society so that we, as a society, have a benchmark to evaluate the price of pharmaceutical products. QALYs are an apples to apples or a foot to foot way to compare the value of drugs for we the people. I mean, is this drug amazing and we should all pay a lot for it? Or is the drug more expensive than the current standard of treatment and it doesn’t confer any added benefit to patients? It’d be good to know that as a patient and as a payer and, frankly, as a pharma company. QALYs offer a framework for levelheaded discussions. It’s complicated. I’m gonna take the risk of oversimplifying, but here’s how I’d explain the three parts in a QALY measurement, which combines measure pharmaceutical value. The first part is, if relevant, how much additional survival can be expected with this drug? So, if it’s an oncology drug, for example, how much longer will the patient live? The second part of a QALY is, how does the drug make the patient feel? So, in an ideal world, survival is long and the patient feels super great. So, some economists and scientists get together and they do some math and they come up with the sum of these first two factors. Then the third part of a QALY calculation is the cold hard cash. How much is society willing to pay for this improvement in survival, in quality of life? This last part will depend based on the society (ie, the country) and also the condition. We’re willing to pay a lot for a drug that helps blind people see. We might be not so willing to pay a whole lot for a drug that lowers blood pressure marginally, for example. My guest in this health care podcast is Anna Kaltenboeck. She is a health economist and program director for the Drug Pricing Lab at Memorial Sloan Kettering. She knows a lot about QALYs. One last thing: ICER is the Institute for Clinical and Economic Review. It is an independent and nonprofit organization who creates a lot of these QALY assessments. Whether they succeed or not is something that is sometimes questioned, but the team over at ICER prides themselves in not working for Pharma and not working for payers in an effort to be as impartial as possible.   You can learn more at drugpricinglab.org.   Anna Kaltenboeck is the senior health economist and program director for the Center for Health Policy and Outcomes and the Drug Pricing Lab at Memorial Sloan Kettering Cancer Center (MSKCC). She focuses on the development and application of reimbursement methods for prescription drugs that reduce distortionary incentives in the supply chain and encourage pricing of treatments based on their value. Her work centers on developing an unbiased evidence base that characterizes the effect of federal policies on coverage and reimbursement decisions for branded specialty drugs and cell and gene therapies and identifying opportunities for policy changes that encourage affordability and access while maintaining incentives for innovation. Her current research interests include global comparisons of reimbursement policy and supply chain regulation, game theory in innovation decisions, and the effect of market concentration on pricing decisions. Ms. Kaltenboeck’s research and policy work is informed by her experience as a consultant for pharmaceutical clients. Prior to joining MSKCC, Ms. Kaltenboeck spent 10 years working for Analysis Group and IMS Consulting Group, where she conducted health economics and outcomes research and developed pricing and market access strategies for pharmaceutical and diagnostic products. She has published numerous articles in peer-reviewed journals and other press, including JAMA and Morning Consult, and speaks frequently on the topics of value-based pricing, economics of the supply chain, and reimbursement models. Ms. Kaltenboeck holds bachelor’s and master’s degrees in economics from Tufts University. 3:56 What is a QALY? 05:28 “You don’t get marks; it’s the treatment that gets the marks.” 09:13 What is willingness to pay? 10:52 “What we pay for drugs should be reflected in societal preference.” 12:29 Does Pharma fear the QALY? 15:38 “At the end of the day, the ideal here is simply to be able to quantify ‘This is what we’re going to pay for this additional benefit that we’re going to provide for patients.’” 17:09 “When you meet that price, patients should be getting access to that product.” 19:27 What are the significant advances being seen with QALYs and drug development? 21:23 “The challenge is when the price is so much higher than those benchmarks.” 22:27 How do we use the QALY as a tool? 25:56 Where does value-based pricing fall in the world of QALYs? You can learn more at drugpricinglab.org.   @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue What is a #QALY? @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue “You don’t get marks; it’s the treatment that gets the marks.” @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue What is willingness to pay? @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue “What we pay for drugs should be reflected in societal preference.” @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue Does Pharma fear the QALY? @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue “At the end of the day, the ideal here is simply to be able to quantify ‘This is what we’re going to pay for this additional benefit that we’re going to provide for patients.’” @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue “When you meet that price, patients should be getting access to that product.” @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue How do we use the QALY as a tool? @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue Where does value-based pricing fall in the world of QALYs? @a_kaltenboeck discusses #drugpricing and #patientadvocacy in this week’s #healthcarepodcast. #healthcare #podcast #digitalhealth #healthtech #healthvalue #drugvalue

Dr Virgilio Sacchini is a professor of surgery at Memorial Sloan Kettering Cancer Center in New York and the University of Milan.

In this episode, Dr. Diane Reidy-Lagunes chats about recent findings regarding the benefits of exercise, in the prevention and treatment of cancer. She speaks with Lee Jones, exercise scientist at MSK, and Charlie Sweeney, marathon runner and cancer survivor.  For more information and to ask a question, please visit MSKCC.org/podcast See omnystudio.com/listener for privacy information.

In this episode, Dr. Diane Reidy-Lagunes talks to medical oncologist and scientist Jedd Wolchok and cancer survivor Grace Dunn. Together, they help decode the emerging new defense against cancer: immunology. For more information and to ask a question, please visit MSKCC.org/podcast See omnystudio.com/listener for privacy information.

To date, a select number of myeloma patients have become COVID-19 positive. What have they experienced and how have they fared? Dr. Ola Landgren of Memorial Sloan Kettering Cancer Center is living in New York City, a major hot spot in the United States for COVID-19. He joins us on HealthTree Podcast for Multiple Myeloma to share his expderiences in treating COVID-19 positive patients and his suggestions for myeloma patients who have not been infected with COVID-19. Join us for this relevant and important program during this critical time for myeloma patients.  Thanks to our episode sponsor, Takeda Oncology. 

Mi experiencia en MSKCC por Julia Ruiz que tuvo lugar el 10 de Junio de 2016 en Málaga a cargo de la Asociación de Oncología Integrativa ORGANIZADO POR—————————— Asociación Oncología Integrativa http://oncologiaintegrativa.org/web/ ————————————INFORMACION SOBRE MINDALIA—————————— Mindalia.com y Mindalia Televisión son una ONG SIN ANIMO DE LUCRO Si te ha gustado este video, APOYANOS CON UNA DONACION: https://www.paypal.com/cgi-bin/webscr?cmd=_s-xclick&hosted_button_id=G58CS4AVKC6BU SUSCRIBETE AL CANAL DE YOUTUBE para no perderte ningún video: http://www.youtube.com/subscription_center?add_user=mindaliacom MILES DE VIDEOS de conferencias y entrevistas de interés en http://www.mindaliatelevision.com Participa en las CONFERENCIAS EN DIRECTO: http://television.mindalia.com/category/conferencias-en-directo/ -Puedes escuchar este y otros audios en Ivoox: http://mindaliacomradio.ivoox.com PIDE O ENVIA AYUDA http://www.mindalia.com – La Red Social de Ayuda a través del Pensamiento SIGUENOS EN REDES SOCIALES: -Youtube: http://www.youtube.com/mindaliacom -Facebook: https://www.facebook.com/mindalia.ayuda/ -Twitter: http://twitter.com/mindaliacom -Pinterest: https://es.pinterest.com/mindaliacom/ DESCARGATE LAS APLICACIONES MOVILES GRATUITAS: Mindalia Multimedia https://play.google.com/store/apps/details?id=es.app.mindalia_television Mindalia Red de Ayuda https://play.google.com/store/apps/details?id=es.app.mindalia_ayuda&hl=es CONTACTA CON NOSOTROS: http://television.mindalia.com/contacto/ -Skype: mindalia.com ¿Tienes un video que te gustaría que publicáramos? Envíanoslo!!

Listen to our next show with Dr. Sergio Giralt of the Memorial Sloan-Kettering Cancer Center to hear about his deep expertise in transplantation and his latest trials including the use of a vaccine in combination with transplant and a gene-targeted approach using cabozantinib.