Podcasts about gleevec

Based on the latest Novartis Earnings Call that took place on April 23, 2024, the company has provided insights into their strategic positioning and overall direction, specifically in relation to their role in the chronic myeloid leukemia (CML) treatment market. During the call, CEO Dr. Vasant Narasimhan revealed an optimistic outlook for Novartis's progress, projecting that the company could perform at almost three times the level of a previous launch. This projection is based on Novartis's prior success navigating the complex cancer treatment landscape and the established popularity of their drug, Gleevec. With a two-thirds market share of first-line treatments for CML, Gleevec's effectiveness as a tyrosine kinase inhibitor (TKI) has made it a linchpin in Novartis's treatment portfolio.The company also acknowledged that patients often face challenges accessing second-generation TKIs due to systemic barriers. In response to this, Novartis introduced a new drug, Scemblix, backed by a strong patent estate and comprehensive data set. As stated on the earnings call, Scemblix is positioned as a first alternative for CML patients with access issues, marking Novartis's strategic move to drive growth and extend their market impact.Furthermore, as revealed in the call, Novartis is not limited to focusing on third-line treatments. The company plans to strengthen its presence in second-line treatments also. Discussing potential uptake, Dr. Narasimhan observed, "We would expect, I would say, a modest early uptake because we would have to work through -- CML is one of the few cancer areas that's currently contracted. ... we believe that given the overall data set that we'll share at ASCO that it should be able to drive very strong uptake." This perspective illustrates Novartis's aim to reach more of the CML treatment community.Additionally, Medicare's exclusion from Novartis's lifecycle management agreements was signaled out on the call, representing a strategic move that could significantly shape CML treatment options. This exclusion opens up additional treatment possibilities beyond generic imatinib for a sizeable group of CML patients, highlighting yet another way Novartis anticipates influencing the market dynamics of CML treatments.In summary, Novartis's earnings call outlined several strategic considerations, including tackling access problems, exploring new market segments, and solidifying their product lineup. These efforts demonstrate Novartis's focused attempt to maintain and potentially enhance their role within the CML treatment spectrum, albeit tempered by the reality of the unknown complexities within the healthcare landscape. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit www.theprompt.email

When Tim Sohn spotted some unusual bruises on one of his legs, he sought medical attention.  This led to hospitalization and a subsequent diagnosis of a form of blood cancer, chronic myeloid leukemia.  With the aid of two types of oral chemotherapy, Tim survived.  His experience inspired him to help others diagnosed with cancer, in the form of a book and a live podcast.  This is his story.

Mel Mann was diagnosed with a cancer known as CML and given three years to live. That was in 1995. Today, in 2023, Mel Mann is still living and still advocating – all thanks to accelerated approval and a clinical trial. Hear the story of how this Army vet, and longest-living Gleevec patient, beat the odds and stands here today. And Terry and Bob discuss the brand new accelerated approval report that Patients Rising released. Unprecedented coverage decisions from CMS, the history of accelerated approval, and why it's such an essential pathway for patients are all in today's episode. The Mel Mann Story: From Terminal Cancer to 28 Year Survivor (Long Version) Connect with Mel Mann on Twitter Patients Rising Now Accelerated Approval Report ADA Anniversary   Need help? The successful patient is one who can get what they need when they need it. We all know insurance slows us down, so why not take matters into your own hands? Our Navigator is an online tool that allows you to search a massive network of health-related resources using your zip code so you get local results. Get proactive and become a more successful patient right now at the Patients Rising Helpline. Have a question or comment about the show, or want to suggest a show topic or share your story as a patient correspondent? Drop us a line: podcast@patientsrising.org The views and opinions expressed herein are those of the guest(s)/ author(s) and do not reflect the official policy or position of Patients Rising, nor do the views and opinions stated on this show reflect the opinions of a guest's current or previous employers.  

MacKay Jimeson, Acting Executive Director of Patients Rising Now, previews Monday's accelerated approval hill briefing, which is open for staff to attend; Mel Mann, the longest-living Gleevec patient, discusses how accelerated approval saved his life and will speak at Monday's hill briefing. Sign Up: The Value of Accelerated Approval for Patient Access & Medical Advances House Energy and Commerce Committee: Chair Rodgers Opening Statement on Spurring Lifesaving Medical Innovation The Mel Mann Story: From Terminal Cancer to 28 Year Survivor (Long Version) Patients Rising Podcast  

Synopsis: Bill Hinshaw is the President and CEO of Axcella Therapeutics, a clinical-stage biotechnology company pioneering a new approach to treat complex diseases using endogenous metabolic modulator (EMM) compositions. Bill entered biotech a little over four years ago following a long life sciences career in pharma, working for companies such as Novartis and Schering Plough. He joins host Rahul Chaturverdi for a discussion about where Axcella is from a development perspective and the therapeutic areas they're pursuing, the company's work to treat long Covid, the challenges of developing drugs to treat nonalcoholic steatohepatitis (NASH), and Axcella's “combination by design” multi-targeted approach to tackle complex diseases. Read More on Axcella Announces Positive Interim Data from Phase 2b EMMPACT Study of AXA1125 in Nonalcoholic Steatohepatitis (NASH) https://bit.ly/3U0iEa6 Biography: Mr. Hinshaw joined Axcella as CEO in May 2018. He is the former Executive Vice President of U.S. Oncology at Novartis Pharmaceuticals Corporation, having served 15 years with the organization. Mr. Hinshaw led all aspects of this >$6B organization, heading up more than a dozen product launches, including Tasigna®, Gleevec®, and Kymriah®; the integration of the GSK oncology portfolio; innovative medical, commercial, and market access models; and a patient-centric focus on education and support programs. He also played a key role on the Global Oncology Executive Committee, including leading key strategic programs to maximize the portfolio and pipeline development. Mr. Hinshaw was formerly the Head of the Northern and Central Europe Region for Novartis Oncology where he was responsible for leading all functions across 33 countries. Prior to that role, Mr. Hinshaw was the head of Group Emerging Markets, which included all divisions of Novartis in 50 countries worldwide. Prior to his role as EVP, Mr. Hinshaw held a number of lead roles for Novartis, including Head of the Hematology Business Franchise, which achieved >20% overall growth each year under Mr. Hinshaw's leadership. He also was the Global Head of Infectious Disease and Transplantation and Immunology (IDTI) based out of Basel, Switzerland, with responsibility for all functions of the organization, including commercial, development, BD&L, and strategy for the Business Unit. Other Novartis positions held by Mr. Hinshaw included Global Head of Infectious Disease Marketing and IDTI Development and Business Development & Licensing; Business Franchise Head, Infectious Disease; and Head of Infectious Disease Marketing. Mr. Hinshaw started his career at Schering Plough, where over the course of 12 years, he held a series of roles of increasing responsibility in the sales and marketing functions in both primary care and specialty business units, including market research, new products and in-line brand management, and sales positions at the representative, district, regional, and national levels. He also led the U.S. Oncology Unit where he was responsible for sales, marketing and business development. Mr. Hinshaw holds a B.S. in Molecular Biology from the University of Wisconsin.

Today Gleevec is an incredibly common cancer treatment.  But like every drug on the market, it went through clinical trials more than two decades ago.  Our guest today, Mel Mann, was the second person to receive the drug, back in 1998. And it saved his life.Mel was diagnosed with chronic myeloid leukemia, (CML) in 1995 and was given three years to live.  At the time, a bone marrow transplant was the only option. The registry had far less people on it than today, particularly people of color.  At the time, only 1% of black patients could find a match.  So Mel, an Army Major at the time, did what he did best--with boots on the ground, he started organizing bone marrow drives - everywhere. And he enlisted his incredible friends to do the same.And while Mel didn't find a match, it was a chance meeting at a relative's drive that would change his life forever.  He takes us through the series of events that introduced him to a clinical trial for Gleevec, and just in time.  He ended up not needing a transplant. Mel is proud to say he not only got to see his daughter, five years-old when Mel was diagnosed, grow up but she has also become a doctor. We spend some time with Mel talking about clinical trials, and how important, even life-saving they can be.  As a patient, you truly need to be your own best advocate and Mel will show you the way.More:US Clinical Trials Website: https://clinicaltrials.gov/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/nbmtLINKnbmtLINK YouTube Page can be found by clicking here.Thank you to this season's sponsors:Omeros Corporation: https://www.omeros.com/Incyte: https://www.incyte.com/

This month, Cancer History Project guest editor Deborah Doroshow, MD, PhD is conducting several oral histories with people who have experienced cancer—in a preliminary attempt to begin to capture some of those experiences. Although sources regarding the experiences of scientists and clinicians are often readily available, sources documenting the patient experience—a topic which historians of medicine like myself are deeply committed to elucidating—tend to be more difficult to find and are less frequently saved by archivists. Doroshow's first oral history is with Judy Orem, a participant on the phase I clinical trial of (Imatinib), or Gleevec. While the story of Gleevec's discovery and clinical testing is well known, Judy's narrative provides a new perspective into the experience of being one of the first people to participate in a clinical trial of one of the earliest targeted therapies in hematology and oncology. A transcript of this podcast is available here.

When unnamed Bloomberg sources said that Dexcom is in talks to buy Insulet in what could be the year's biggest medtech megamerger, stock prices went wild. And the American Society for Clinical Oncology annual meeting, the biggest cancer conference, will be held in June, but we have early news to share. Also under discussion is the new monkeypox outbreak, what the treatment options are and why health officials don't seem concerned. Lastly, nominations are finally open for the annual Fierce 15 competition. We'll hear from the judges about what it takes to make your nomination stand out from the rest.    To learn more about the topics in this episode: Roche rolls out trio of PCR research tests for monkeypox Bavarian Nordic signs 'larger' monkeypox vaccine supply deal with unnamed country US to provide Bavarian Nordic's vaccine Jynneos to some at risk for monkeypox, CDC says Moderna tunes vaccine platform to next potential viral threat: monkeypox Monkeypox outbreak won't be the next global pandemic thanks to vaccines, drugs: analysts Dexcom, Insulet in talks to merge into a diabetes device behemoth: report Biohaven flunks first clinical test for rare disease drug post-Pfizer sell-off ASCO: Is another pan-tumor drug on the horizon? Johnson & Johnson thinks Balversa could be it ASCO: J&J, Legend reveal more CAR-T data and a look at Carvykti for earlier myeloma in a difficult population ASCO: J&J's multiple myeloma toolkit expands with bispecifics data ASCO: Novartis eyes full nod for Gleevec follow-on Scemblix thanks to new leukemia data GSK dodges UK strike with improved pay offer for staffers Calling all Fierce 15 fans: Nominations for the 2022 Fierce Biotech Fierce 15 are now open The Top Line is produced by senior multimedia producer Teresa Carey with editor-in-chief Tracy Staton, managing editor Querida Anderson and senior editors Annalee Armstrong, Ben Adams, Conor Hale and Eric Sagonowsky. The sound engineer is Caleb Hodgson. The stories are by all our “Fierce” journalists. See omnystudio.com/listener for privacy information.

“I'm in a part of my life where I like to have an impact that disrupts an industry,” says famed entrepreneur Mark Cuban, and his new online pharmacy CostPlus Drugs is already showing signs of creating a major disruption, indeed. Here's just one example of what his no-frills operation is making possible: a 30-day supply of the cancer-fighting drug Gleevec is usually $2,500, but on CostPlusDrugs.com the same medication is $17.10 for a month's supply.  You probably have the same question as host Shiv Gaglani: how is this possible? Cuban says CostPlus Drugs sidesteps insurance companies and Pharmacy Benefit Managers to deal directly with manufacturers.  There's a standard 15% markup to cover operational costs, a $3 pharmacy fee and a $5 shipping fee. “That's it, period, end of the story.” Word of mouth over the last two months has pushed sales to levels not expected for two years. Cuban is quick to credit co-founder Alex Oshmyansky and his team, but obviously the business acumen he's displayed for years on the TV show Shark Tank plays a big role, as does his motivation to do something about a bedeviling problem. “The fact that people are having to choose between rent, food, or medication in this country is wrong in every which way.” Check out this fascinating analysis of the healthcare industry spiced with valuable advice for budding healthcare entrepreneurs, and find out what Cuban thinks the healthcare industry can learn from the NBA. Mentioned in this episode: https://costplusdrugs.com/

On the show today I speak with Mel Mann, the longest living person who participated in the clinical trial for Gleevec. When Mel Mann was diagnosed with chronic myeloid leukemia at age 37 in 1995, he was told he had three years to live. But he's here some 26 years later and still going strong. Mel served as a major in the U.S. Army. He kickstarted blood marrow drives all across the country. He started running marathons to raise money for cancer research. He went back to school to become a high school English teacher. And now Mel serves as a cancer advocate and patient activist. He's here to talk about his epic journey.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Professor Norbert Gattermann, a hematologist and medical oncologists joins the podcast for the first of two episodes in this edition of the PV Roundup specialist spotlight.

Twenty years ago, Dr. Charles Sawyers played a pivotal role in the development of Gleevec, a game-changing cancer drug that has gone on to save millions of lives and open doors for research and innovation. In this episode, Dr. Diane Reidy-Lagunes talks with Dr. Sawyers about what's next in the field of cancer pharmaceuticals. Is another silver bullet on the horizon? See omnystudio.com/listener for privacy information.

In this episode of the “CURE® Talks Cancer” podcast Mel Mann discusses his participation in the clinical trial for Gleevec and how it changed the trajectory of his life.

Arundhati interviewed Sarah Boyce, CEO of Avidity Biosciences. In October 2019, Sarah Boyce joined Avidity as President and CEO, and she serves as a member of the board of directors. Ms. Boyce brings to Avidity extensive operational, commercial and leadership experience in the life sciences industry and has built global organizations, bringing a number of innovative therapies including Tegsedi®, Waylivra®, Soliris®, Gleevec® and Tasigna® to patients. Episode Resources Connect with Arundhati Parmar aparmar@medcitynews.com https://twitter.com/aparmarbb?lang=en https://medcitynews.com/ Connect with Sarah Boyce https://www.linkedin.com/in/sarah-boyce-7775808/ http://www.aviditybiosciences.com/about-us/ 

Before 2001, a diagnosis of chronic myelogenous leukemia was almost certainly terminal. But a breakthrough drug pioneered by a doctor at OHSU changed that and made the rare cancer treatable, saving thousands of lives.  Dr. Brian Druker, chairman of OHSU's Knight Cancer Institute, and Rob Shick, a CML survivor and chair of the Knight Cancer Council, join Laural Porter to celebrate the 20th anniversary of Gleevec's FDA approval, look back on the impact it has had on cancer care, and discuss what's next in the fight to cure cancer. 

La mutagenèse somatique : le cancer dériverait d'une simple cellule dont l'ADN a muté ce qui la rendrait immortelle. On a dépensé des milliards pour arriver à isoler 100 « oncogenes » et un peu plus de 15 gênes suppresseur de tumeur. L'institut pour le cancer américain a un budget de 5,74 milliards de dollars (publics). Où est-ce que ces recherches nous ont emmené ? C'est une vrai question que je me pose lorsque je constate que la mortalité liée au cancer ne cesse d'augmenter. Serais-ce parce que nous aurions justement focalisé sur l'arbre qui nous empêche de voir la forêt ? Toutes nos cellules n'existent jamais en dehors de nos tissus ! Toutes nos cellules sont issues d'un seul ovocyte fertilisé et donc partage exactement le même ADN. Ce ne serait donc pas la cellule qui est à l'origine de la différenciation cellulaire mais c'est ses tissus environnants, et c'est lié à des phénomènes de signaux hormonaux. La recherche actuelle focalise sur la cellule pour savoir quel gêne a muté. Mais alors comment se fait-il alors que toutes les cellules de notre corps ne deviennent pas cancéreuses ? C'est la graine ou le sol le problème ? Par analogie, la recherche médicale actuelle focalise sur la graine tandis que le vitalisme focalise sur le sol. Chaque cellule de notre corps peut devenir « cancéreuse » c'est donc la preuve que c'est une propriété innée de nos cellules. La graine du cancer est présente dans chacune de nos cellules, ce n'est donc pas la graine qui importe, mais le sol. Le sol s'apparente à notre environnement. Quel environnement favorise la multiplication des cellules a un niveau de mutation qui dépasse largement le niveau de mutation « normal » d'une cellule ? Exemple du Gleevec : c'est un médicament qui est présenté comme une avancée majeure dans la lutte contre le cancer. C'est un bloquant de la protéine kynase. Il vient affecter le sol (les signaux de croissance dans le corps) pas la graine ! Cela n'invalide pas toute la recherche génétique, cela montre juste que cela ne sert à rien pratiquement sinon à engloutir des quantités astronomiques de fonds publics. Le vivant EST son environnement. This podcast is published by H/M Collection, a reinformation channel aiming to collect and provide multiple media content of different creators in topics of Society & Culture, News & Politics, Religion & Eschatology. Support the show on https://www.patreon.com/hmcollection for as little as 1€ a month.

On the show today, I welcome one of my advocate heroes, Erin Zammett-Ruddy, a young adult cancer survivor I met during the LIVESTRONG days in the early 2000s. She may have barely crossed the 5-year survivor finish line (that’s what we called it back then), but she was — and still is — a force to be reckoned with. She was a “big-time big city” magazine journalist writing for Glamour when a random asymptomatic diagnosis of Chronic Myelogenous Leukemia changed everything. She broke the mold and went public — something considered shocking for the time — and began a now legendary and award-winning column entitled “Life with Cancer" — making her one of the first media cancerlebrities of all time. There’s so much to unpack with Erin, the least of things her choice to temporarily quit chemo to become a biological mom, confronting her sister’s cancer diagnosis two years after her own, maintaining her career, speaking all over the world, raising a shit ton of money for charity — you get the picture. Now a happily thriving 40-something raising three kids and married to the same man who stuck with her during the dark days, Erin’s still here and kicking more ass than ever with her new book, “The Little Book of Life Skills: Deal With Dinner, Manage Your Email, Make a Graceful Exit, and 152 other Expert Tricks". Enjoy the show.

Retiring ASCO Chief Medical Officer Dr. Richard L Schilsky gives a far-reaching interview with ASCO in Action podcast host ASCO CEO Dr. Clifford A. Hudis, who examines Dr. Schilsky’s trailblazing medical career, his leadership in ASCO and indelible mark on its research enterprise, and what he sees for the future of oncology. ASCO’s first-ever Chief Medical Officer even offers some friendly advice for Dr Julie Gralow, who starts as ASCO’s next CMO on February 15, 2021. In a touching tribute, Dr. Hudis also shares what Dr. Schilsky’s friendship and mentorship has meant to him personally, and suggests that Rich will still be supporting ASCO on critical priorities moving forward. Don’t miss this exchange with one of oncology’s greats! Transcript 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. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. CLIFFORD HUDIS: Welcome to this ASCO in Action podcast brought to you by the ASCO Podcast Network, a collection of nine programs covering a range of educational and scientific content and offering enriching insights into the world of cancer care. You can find all of the shows, including this one, at podcast.asco.org. The ASCO in Action podcast is a series where we explore the policy and practice issues that impact oncologists, the entire cancer care delivery team, and the individuals we care for-- people with cancer. My name is Dr. Clifford Hudis. And I'm the CEO of ASCO and the host of the ASCO in Action podcast series. For today's podcast, I am especially pleased to have as my guest my friend, colleague, and mentor Dr. Richard Schilsky, ASCO's chief medical officer. Now, I am sure that many of our listeners have already heard that Dr. Schilsky will be leaving ASCO in February of 2021, retiring. However, I want to reassure everybody that even in retirement, he will continue to make contributions and provide leadership to all of us. And his illustrious and path-blazing career in oncology spanning more than four decades is not quite over thankfully. Rich is ASCO's first chief medical officer. And as such, he has made a truly indelible mark on all of us. He started with a proverbial blank piece of paper. The position had no precedent. It had no budget. It had no staff. But now after just eight years in the role, he has helped make the CMO a critically important position at the society. And I have to say that success is more than anything due to Rich's vision and his leadership. And that's some of what we'll be talking about today. So Rich, thank you very much for joining me today for what I hope is going to be a great casual but informative conversation about your amazing career, your unique role at ASCO, and maybe most importantly in the end what you see for the future of oncology not just in the United States, but around the world. Thanks for coming on, Rich. RICHARD SCHILSKY: Thanks, Cliff. It's great to be here today. CLIFFORD HUDIS: So with that, let's just dive right in and start at the very beginning. Rich, tell everybody why you decided to become an oncologist and maybe share a little bit about what those early days looked like for you and, in that context, what it was like to have cancer at the beginning of your career. RICHARD SCHILSKY: Well, I knew from an early age that I wanted to be a doctor. And in fact, I had written a little essay when I was in sixth grade as a homework assignment called My Ambition. And my mother had tucked that away in a scrapbook. And I found it a number of years ago. And on rereading it, it was quite amazing to me to see what I was thinking about even then. Because I said not only did I want to be a doctor, but I didn't think that was enough, that I wanted to be a medical researcher because I wanted to discover new information that would help people heal from whatever their diseases might be. And so it was never really any doubt in my mind that I would be a physician. I went to medical school at the University of Chicago. But I was living in New York City at the time having grown up in Manhattan. And the only year we had off in medical school, the only time we had off in medical school, was the summer between the end of the first year and the beginning of the second year. So during that time, I went back to Manhattan. And I was able to get a fellowship from the American College of Radiology that allowed me to essentially hang out in the radiation therapy department at New York University Medical Center, which was within walking distance of where I grew up. And so I would go over there every day. And I was taken under the wing of a young radiation oncologist. And of course, I wasn't really qualified to do anything at that point except to follow him around, talk and listen to the patients. But that turned out to be a really formative experience for me because we saw the whole gamut of cancer. We saw head and neck cancers. We saw lung cancer. We saw patients with breast cancer and prostate cancer. And in those years-- this is the early 1970s-- many of these patients have fairly locally far advanced disease and were quite debilitated by it. But listening to their stories, hearing about their hopes and their struggles, really demonstrated to me the human side of cancer. So I went back to school and thought about this in the context of my own personal experience, which dated back to when I was in college when my mother's mother, my maternal grandmother, was diagnosed with breast cancer. This was 1968. And as you well know, there were very few therapies available for breast cancer in the late 1960s, mostly hormone therapies. And my grandmother had the treatment that was considered standard of care at that time, which was extended radical mastectomy followed by chest wall radiation. And some years after that first mastectomy, she had a breast cancer that developed in the opposite breast and had a second extended radical mastectomy and chest wall radiation. And these were very traumatic and disfiguring procedures for her to go through. Anyway, long story short is after another few years, she developed bone metastases and then brain metastases. And there was really very little that could be done for her other than hormone therapies. And having observed her go through that illness and realizing how limited our treatment options were and then having the experience after my first year in medical school pretty well cemented for me that I wanted to be an oncologist. I thought actually about being a radiation oncologist. But then I did my internal medicine rotation in medical school, fell in love with internal medicine. And that sort of put me on the path to be a medical oncologist. The clinical challenge of caring for cancer patients, the emotional attachment to those patients, and, of course, even then, the unfolding biology of cancer was so intellectually captivating that I actually applied for oncology fellowship when I was a senior medical student. So even before going off to do my medical residency, I had already been accepted as a clinical associate at the National Cancer Institute to start two years hence. And that's how I became an oncologist. CLIFFORD HUDIS: So it's so interesting. Because, of course, the story I'm sure for many people interested not just in oncology, but even medical education, there are little things that don't happen nowadays that happened with you like that last little vignette about the early acceptance into an advanced training program before your fellowship among other things. Can you remind us about the timeline? Because I think one of the things that many of our listeners often can lose sight of is just how new oncology really is as a specialty. ASCO itself founded in 1964. And the first medical oncology boards were mid-'70s, right? So you were in med school just before that second landmark, right? RICHARD SCHILSKY: That's right. I graduated from medical school in 1975. I started my oncology fellowship in 1977. And I got board-certified in medical oncology and joined ASCO in 1980. And so that was the time frame at that point. CLIFFORD HUDIS: So the internal medicine was actually, if I heard you right, just two years, not the now traditional four. RICHARD SCHILSKY: Yeah. I was a short tracker. I did only two years of internal medicine training rather than three. I did my training at Parkland Hospital and University of Texas Southwestern in Dallas with at that time a legendary chair of medicine, Don Seldin, who I had to get permission from him to leave the program prior to completing the third year of residency because I had already been accepted into fellowship at NCI. And he, Seldin, who was a brilliant chairman and a brilliant nephrologist, was not at all interested in cancer. And it took a bit of-- I was going to say arm twisting, but it really took bleeding on my part to get him to agree to allow me to leave the residency program to go to the NCI. But he eventually agreed. And in those years, the first-year clinical fellowship at the NCI was like being an intern all over again. There were about 15 of us. We were on call overnight in the clinical center once every two weeks. We cared for all of our inpatients as well as had a cadre of outpatients. We did all of our own procedures. We had no intensive care unit. So patients who were sick enough to require ventilator support, we cared on the floor in the inpatient service on our own with guidance from senior oncologists. It was a bit different from the way it is now. But, of course, it was fantastic on-the-job training because we just learned a ton and had to learn it very quickly. CLIFFORD HUDIS: So that's actually a great segue to the advances because there was a lot to learn then. But, wow, there's a lot more to learn, I think, now. And I have real sympathy for trainees and younger oncologists for the breadth of what they need to learn. Again, just testing your memory, but platinum came along pretty much in the mid-'70s as well, right? That was a pivotal expansion of the armamentarium for us. So what do you see-- when you summarize progress in cancer research and care over these decades, what do you think are the most pivotal or revolutionary milestones that you identify over the span of your career? RICHARD SCHILSKY: Yeah. It's really interesting to think about it historically. There were the early years of discovery in oncology from the 1950s to the 1970s when we really had the introduction of the first chemotherapy drugs and the miraculous observation that people with advanced cancer could actually obtain a remission and, in some cases, a complete remission with chemotherapy and combination chemotherapy in particular. And so that was the formative years of oncology as a medical specialty and really proof of concept that cancer could be controlled with drugs. When we got into the 1980s, the 1980s in many respects were the doldrums of progress in clinical oncology. There really was not a lot of innovation in the clinic. But what was happening and what was invisible to many of us, of course, was that was the decade of discovery of the fundamental biology of cancer. That's when oncogenes were discovered, when tumor suppressor genes were discovered, when it became clear that cancer was really a genetic disease. And that is what transformed the field and put us on the path to targeted therapy and precision medicine as we think of it today. So I think that clearly understanding the biology of cancer as we do now and all that it took to lead us to that point, which was a combination of understanding biology, developing appropriate technology that would, for example, enable the sequencing of the human genome and then the cancer genome. And the other formative technology in my opinion that really changed the way we care for cancer patients was the introduction of CT scanning. When I was still a fellow at the NCI, we did not have a CT scanner. If we needed to get detailed imaging of a patient, we did tomography. And if you remember what tomograms looked like, they were really blurry images that you could get some depth perception about what was going on in the patient's chest or abdomen. But they really weren't very precise. When CT scanning came along, it really revolutionized our ability to evaluate patients, assess the extent of disease, stage them in a much more precise way, which then allowed for better patient selection for curative surgery, better radiation therapy planning. So we don't often point to imaging advances as some of the transformative things that paved the way in oncology, but I think imaging is really overlooked to some extent. So I think the technology advances, the biological advances, are the things that really allowed the field to move forward very quickly. And by the time we got into the mid-1990s, we were beginning to see the introduction of the targeted therapies that have now become commonplace today. And then it was around 2000, I think, that we saw the introduction of Gleevec. And I'm reminded always about an editorial written by Dan Longo in The New England Journal a few years ago. And Dan and I were fellows together. We worked side by side on the wards at the clinical center and became very good friends. And Dan in his role as a deputy editor of The New England Journal wrote an editorial a few years ago that was titled "Gleevec Changed Everything." And Gleevec did change everything. It changed our entire perception of what were the drivers of cancer and how we might be able to control cancer very effectively and potentially put it into long-term remission. Now, of course, we know now that the whole Gleevec story is more of an exception than a rule in targeted therapy. And, of course, we know that tumors become resistant to targeted therapies. But we couldn't have known any of this back in the early years of oncology because we had no real insight into what caused cancer to grow or progress. And the notion of drug resistance, while we realized that it occurred, we had no idea what the mechanisms were. So it's such a different landscape now than what it used to be. It's quite remarkable. CLIFFORD HUDIS: So as you tell the story, there's, of course, a lot of focus on technology, whether it's biology and understanding the key features of malignancy or imaging or more. But what I also note in your story and I want to come back to is the people. And I can't help but reflect on where we are in this moment of the COVID-19 pandemic. Yes, we've moved to telemedicine. Everything can be accomplished via technology. And, yet, the human touch is so important. When we think about being in the room with people, when we think about face to face from the context of career development and your own career, you touched on Dr. Seldin, I think, already from the perspective of internal medicine training. But are there are other mentors or important shapers of your career that you think we should know about? RICHARD SCHILSKY: Well, probably, the most influential person early in my career in medical school was John Altman. John, you may know, was the inaugural director of the University of Chicago's NCI-designated Cancer Center, which was one of the very first NCI-designated cancer centers in 1973 after the National Cancer Act of 1971 created the cancer centers program. And John, who was a leading oncologist studying Hodgkin and non-Hodgkin's lymphoma, was a faculty member there. He was the director of our cancer center as I said. He took me under his wing even when I was in medical school and served as a real role model and mentor to me. When I was in my internal medicine training as I mentioned earlier, Don Seldin, the chair of medicine, was never particularly interested in oncology. So, to some extent, I didn't have-- I had great internal medicine training. But I did not have good mentorship in oncology. When I got to the NCI, then my whole world really opened up. And the two pivotal people there in my career were Bob Young, who was chief of the medicine branch and was my clinical mentor and remains a mentor and friend to this day, and then, of course, Bruce Chabner, who was the chief of the clinical pharmacology branch. And in my second year of fellowship when we all went into the laboratory, I went into Bruce's lab. And that's where I really got interested in the mechanism of action of anti-cancer drugs and ultimately in drug development and early phase clinical trials. And both Bob and Bruce remain very close to me even today. CLIFFORD HUDIS: So I'm concerned about time on our call today on our discussion. Because we could obviously fill lots of hours on all of these remarkable experiences and amazing people you worked with. But I'm going to ask that we fast forward a little bit. You and I share, I think, passion and love for ASCO. So I think that it's reasonable for us to focus a little bit on that for the time we have left here. You didn't start out obviously as chief medical officer at ASCO. But you were a really active ASCO volunteer and leader. Maybe tell us a little bit about some of the ASCO volunteer roles that you engaged in and what that meant to you at the time and how that led to this role. RICHARD SCHILSKY: Well, I'll be brief. I joined ASCO in 1980 at the first moment that I was eligible to join ASCO. I had attended my first ASCO meeting the year before, 1979, when I was still in my fellowship training. And it was clear to me even then when the whole annual meeting was about 2,500 people in two ballrooms in a hotel in New Orleans that that was a community of scholars and physicians that I wanted to be a part of. And so, over the years, I did what people do even today. I volunteered to participate in whatever ASCO activity I could get involved with. Over the years-- I think I counted it up not too long ago-- I think I served or chaired 10 different ASCO committees, more often serving as a member, but in a number of those committees also serving as the chair over many years. And as I became more deeply involved in ASCO and saw other opportunities to engage, I had the opportunity to run for election to the board and was-- after a couple of tries was elected to serve on the board and then eventually elected to serve as ASCO president in 2008-2009. But the attraction of ASCO in many ways was a community of diverse but, in many ways, like-minded people, people who had similar passion and drive and focus. But I think what you get at ASCO in many ways is the wonderful diversity of our field. If you work in a single institution for much of your career as I did and as you did, you get to know that institution pretty well. You get to know its perspectives and its biases and its strengths and its weaknesses. But there's a whole world of oncology out there. And you can get exposed to that at ASCO because you meet and work with colleagues from every clinical setting, every research setting, people who have remarkable skills and interests and passions. And it's just a wonderful environment to help develop your career. So I consider myself to be extremely fortunate to have had the journey in ASCO that I've had culminating, of course, with ultimately my coming on the staff as ASCO's first chief medical officer. CLIFFORD HUDIS: We often joke about that blank sheet of paper. But in retrospect, it's very obvious that you had built up that collection of LEGO blocks, and then you assembled them all into the ASCO Research Enterprise, a name you gave it. And it really, in retrospect, builds, I think, very cleanly upon all of your prior experience, but also the vision that you developed based on that experience for how research should be conducted. Can you maybe share with everybody the scope and vision for the ASCO Research Enterprise, what the intent was, and where you see it going, and what it includes today? RICHARD SCHILSKY: Sure. I won't claim that I came to ASCO with the whole thing fully developed in my mind. As you said, when I came, I literally did have a blank slate. Allen Lichter, who hired me, said, come on board and help me make ASCO better. And so I, in a sense, reverted to what I knew best how to do, which was clinical research. And having in my career been a cancer center director, a hem-onc division chief, a cooperative group chair, I had a lot of experience to draw on. And it was obvious to me that ASCO was fundamentally an organization that took in information from various sources, evaluated it, vetted it, collated it, and then disseminated it through our various channels, most notably our meetings and our journals. But ASCO itself did not contribute to the research enterprise. And that seemed to me to be a lost opportunity. We knew that ASCO had lots of data assets that could be of interest to our members and to the broader cancer community. But they were scattered all around the organization and not particularly well annotated or organized. So we began to collate those. And they are now available to ASCO members on the ASCO data library. I recognized that we did not have an organized unit in ASCO to support or facilitate or conduct research. So, in 2017, we formed the Center for Research and Analytics and brought together staff who were already working at ASCO but scattered in different departments but all people who had an interest in clinical research or research policy and brought them into this new unit, which has really become the focal point for research work at ASCO. We recognized that ASCO members for many years were interested in surveying their colleagues, surveying other ASCO members, to help advance research questions. But ASCO actually had a policy that prohibited that. So that never really made good sense to me. It seemed like a lost opportunity. And we were able to create a program and have the ASCO board approve it whereby any ASCO member could opt in to participate in what we now call the Research Survey Pool. And in doing so, they are essentially agreeing to participate in research surveys conducted by their colleagues. So that program is now up and running. There are, I think, eight surveys that have been completed or are currently in the field. And this is now a service that ASCO provides through CENTRA to its members to enable them to survey their colleagues for research purposes. Most importantly, I think we saw an opportunity back in 2014 or 2015 to begin to learn from what our colleagues were doing in clinical practice as they began to deploy precision medicine. And there was a lot of genomic profiling that was going on at that time. It was revealing actionable alterations in roughly 30% or so of the tumors that were profiled. But there was a lot of difficulty in doctors and patients obtaining the drugs that were thought to be appropriate to treat the cancer at that particular time because most of those drugs would have to be prescribed off label. And there was not a sufficient evidence base to get them reimbursed. And, moreover, even if they could be reimbursed, there was no organized way to collect the patient outcomes and learn from their experiences. So that led to us developing ASCO's first prospective clinical trial, TAPUR, which really solves both of those problems. Through the participation of the eight pharmaceutical companies that are engaged with us in the study, we are providing-- at one point, it was up to 19 different treatments free of charge to patients. These are all marketed drugs but used outside of their FDA-approved indications. And we were collecting data on the patients, the genomic profile of cancer, the treatment they received, and their outcomes in a highly organized way. And so now this is a study that we launched in 2016. We're now almost to 2021. We have more than 3,000 patients who have been registered on the study, meaning consented to participate, more than 2,000 who have been treated on the study. And we are churning out results as quickly as we can about which drugs are used or not useful in the off-label setting for patients whose tumors have a specific genomic profile. So we built all this infrastructure. And having this in place has also then allowed us to respond rapidly to unmet needs. So when the COVID-19 pandemic overwhelmed all of us, and when our members were looking for information about what was the impact of COVID-19 on their patients, one of the things we were able to do because we had CENTRA, because we had a skilled staff and an infrastructure, was to very quickly stand up the ASCO COVID-19 registry, which we launched in April of this year. And there are now about 1,000 patients who've enrolled in the registry from around 60 practices that are participating. And we will follow these patients now longitudinally and learn from their experiences what has been the impact of the COVID-19 illness on them and their outcomes, how has it disrupted their cancer care, and ultimately how that impacts their overall cancer treatment outcomes. So as I now contemplate leaving ASCO after eight years having started with a blank slate, I'm very proud of the fact that I think I'm leaving us with a remarkable infrastructure. We now have a clinical trials network of 124 sites around the country participating in TAPUR that we never had before. We have through the work of CancerLinQ a real-world evidence data generator that is beginning to churn out valuable insights. We have a capacity to survey ASCO members for research purposes. We have an ability to stand up prospective observational registries to gather information longitudinally about patients and their outcomes. We have a core facility in CENTRA with highly skilled data analysts and statisticians that can support these various research activities. So ASCO is now primed, I think, to really contribute in a very meaningful way to the gaps in knowledge that will forever exist in oncology just because of the complexity of all the diseases we call cancer. And that's what I mean by the ASCO Research Enterprise. It is in fact remarkable and, I think, powerful enterprise if we continue to use it effectively. CLIFFORD HUDIS: Well, that's an interesting segue to my next thought, which is really about what comes next. I'll talk about you. But let's start with ASCO first. Your successor, Dr. Julie Gralow, obviously has been announced publicly. She's an accomplished clinician and researcher. She has a known recognized passion for patients, patient advocacy, clinical research through her leadership at SWOG but also health care equity and global oncology. So from your perspective, having created all of these assets and resources, what advice would you give Dr. Gralow publicly on how to make the position hers, what to take us to next? And I do want to acknowledge for everybody listening that the hints I've been making up until now are that Rich has agreed that he will continue to contribute as a leader to TAPUR for the short term, at least, at least the next year helping Julie get fully oriented to this program and others. So what will your advice be to Julie? RICHARD SCHILSKY: That's a great question. She's a great selection. And congratulations on hiring her. I think there are two key issues, I think, maybe three. One is to have a broad scope and cast a wide net. Oncology care and cancer research and cancer biology are incredibly complicated and nuanced and broad in scope. And although Julie is an accomplished breast cancer clinician and researcher, in this role at ASCO, you have to be very broad. You have to understand all of cancer care, all of cancer research, all of policy and advocacy not as an expert in necessarily in any one aspect of ASCO's work, but you have to understand the impact of all of those things on cancer care providers and on cancer patients. And it's important to always be looking to the future. The future is going to be here before you know it. And we as a professional society have to prepare our members for that future. So that leads me to the second point, which is listen to the members. The members are the people on the front lines who are delivering care to patients every day. And, fundamentally, ASCO's job is to be sure that our members have all the tools and knowledge and resources that they need to deliver the highest quality care to patients every day. So listening to what they need, what their struggles are, what their burdens are, is extremely important. And then the third thing I would recommend to her is that she get to know the staff and colleagues that she'll be working with. ASCO has a remarkably accomplished, skilled, motivated, passionate staff, many of whom have been with the organization for years, if not decades, who understand what ASCO can and cannot do and who understand what our members need. And she will be well advised to spend a good portion of her first few months on the job just listening and learning from her colleagues. CLIFFORD HUDIS: That's always good advice for anybody making a big career move. But, of course, the wisdom you bring to it is palpable and much appreciated. And I'm sure Julie will be taking your advice. And, by the way, so will I continue to do that even after you make your move. So speaking of your retirement, can you share with us a little bit about what it's actually going to look like for you? Is it about family? Or are you still going to have some professional engagement? Again, I suggest that there might be some already, but maybe you could expand on it. RICHARD SCHILSKY: Yeah. I'm still fully focused on my work at ASCO. And, of course, as you know, when I wake up on February 15, I will no longer be ASCO's chief medical officer. And it's going to be a bit of a rude awakening. Fortunately, I will be able to continue my engagement with ASCO through the TAPUR study as you mentioned. I will, of course, forever be at ASCO member and a donor to Conquer Cancer and be willing to serve the society in any way. I have a number of activities that I've been involved with even throughout my time at ASCO. Not-for-profit boards, for example-- I'm on the board of directors of Friends of Cancer Research. I'm on the board of directors for the Reagan-Udall Foundation for FDA. I plan to continue with those activities as long as they'll have me. I've been serving the last few years on the board also of the EORTC, the large European cooperative clinical research group. And I expect to continue in that role. Beyond that, I will see what opportunities come my way. I think one of the things about retirement if you will that I'm looking forward to is the opportunity to pick and choose what to work on based on what interests me without having the burdens of having a full-time job. On the personal front, of course, we're all looking forward to crawling out from the pandemic. I've basically been locked in my home outside Chicago since March. And I'm looking forward to getting back out to a little bit of a social life. As you know, I have two grown daughters and now three grandchildren, two of whom are in Atlanta, one of whom is near by us in the Chicago area. So looking forward to spending time with them as well. So it will be a change for me to be sure after working as hard as-- I feel like I've worked for really now 45 years since I graduated from medical school. But I also feel like I'm not quite done yet and that I still have ways in which I can contribute. I just feel like at this point, maybe it's time for me to choose how I want to make those contributions and spend a little bit more time doing some other things. CLIFFORD HUDIS: Well, both you and my predecessor, Allen Lichter, are modeling something, have modeled something, that I think is not often discussed but can be very important. For people and for institutions, change is not a bad thing. And setting the expectation that you will pour your heart and soul into something but not necessarily do it alone or forever and not prevent others from taking that role at some point, that's a really-- I think it's a selfless kind of sacrifice in a way. Because, of course, you could stay and do what you're doing for longer. But as you and I have discussed, there is a value for all of us collectively in having fresh eyes and new people take organizations in a new direction. That's how I ended up here frankly. And I think that's the kind of opportunity you're creating right now, something that should be celebrated in my opinion. RICHARD SCHILSKY: Well, thanks. And I couldn't agree more. When I look back at the arc of my career and having all the different kinds of leadership roles that I've had, I basically have made a job change every 8 to 10 years. I was the director of our cancer center for nearly 10 years. I was associate dean for clinical research at the University of Chicago for eight years, another position that I created from a blank slate at that institution. The exception was serving 15 years as a CALGB group chair. But that was a position I really loved and enjoyed and felt like at the end of the first 10 I hadn't quite accomplished everything I wanted to accomplish. But the point is that I think it is both necessary for organizations to have regular leadership change. And it's also refreshing for us as individuals. There gets to a point where you feel like you can do your job in your sleep. And I actually think that's a good time to make a change. Because if that's the way you feel, you're not being sufficiently challenged. And you're probably not being sufficiently creative. And so it's a good time to move on and refresh your own activities and give your organization a chance to bring in someone to hopefully build on whatever you've created and bring it to the next level. CLIFFORD HUDIS: Well, I agree with all that, although I think your comment there about doing the job in your sleep would not apply because I'm pretty confident that the environment and opportunities have continued to evolve in a way that has made it interesting from beginning to end. But you don't have to rebut me on that. I just want to thank you very, very much, Rich. As we set up this podcast, I expected that we would have a really fun and enlightening conversation. And, of course, you did not disappoint. We could talk for much, much longer if we only had the time. On a personal note to you and for the benefit of our listeners, I want to share that Rich has been for me a remarkable friend and mentor and colleague. I first met Rich at the very beginning of my career when my mentor, Larry Norton, pushed me out from Memorial into the larger world. And he did that first and primarily through ASCO and the Cancer and Leukemia Group. Those are really the two places where I was exposed to the world. And through the CALGB, Rich really began to offer me and others, many others, opportunities that shaped careers plural, mine and others. So when I got to ASCO as CEO, Rich was there. And I knew I could always depend on you to be clearheaded, intellectually precise, constructive, visionary. And the thing about you, Rich, is that you never would say yes to anything unless you knew for sure you could do it and indeed, I think, how you could do it. I always share this story which your staff at CENTRA pointed out to me. And I have to admit that I hadn't picked it up myself. But in all the years of now working down the hall from Rich, probably hundreds and hundreds of hours of meetings, he never has taken a note in front of me. And, yet, everything we talk about, every action item we conclude to pursue, they all get done. So I don't know, Rich. You have a remarkable way of organizing your thoughts and your plans, keeping it together, and getting things done. And I'm going to miss that tremendously in the years ahead. So, Rich, I want to say congratulations. Congratulations on reaching this really important milestone in your life. Thank you on behalf of ASCO and the broader oncology community and the patients we care for and their families for making the world a better place. And just as a small thing, thank you for joining me today for this ASCO in Action podcast. RICHARD SCHILSKY: Thank you, Cliff. It's been great. CLIFFORD HUDIS: And, for all of you, if you enjoyed what you heard today, don't forget to give us a rating or a review on Apple Podcasts or wherever you listen. And, while you're there, be sure to subscribe so you never miss an episode. The ASCO in Action podcast is just one of ASCO's many podcasts. You can find all of the shows at podcast.asco.org. Until next time, thank you for listening to this ASCO in Action podcast.

Dr. Parkinson has served as President and Chief Executive Officer of ESSA Pharma Inc. since January 2016, and as a Director of the company since June 2015. Prior to joining ESSA he had been a Venture Partner at New Enterprise Associates, Inc. From 2007 until 2012, Dr. Parkinson served as President and CEO of Nodality, Inc., a biotechnology company focused on the biological characterization of signaling pathways in patients with malignancy. Until October 2007 he was SVP, Oncology Research and Development at Biogen Idec, where he oversaw all oncology discovery research efforts and the development of the oncology pipeline. Previously he had served as VP, Oncology Development, at Amgen and VP, Global Clinical Oncology Development, at Novartis. In those roles he oversaw the successful clinical development of a series of cancer therapeutics, including Gleevec, Zometa, Femara, and Vectibix. Dr. Parkinson worked at the National Cancer Institute from 1990 to 1997, serving as Chief of the Investigational Drug Branch and then as Acting Associate Director of the Cancer Therapy Evaluation Program (CTEP). He is a past Chairman of the Food & Drug Administration (FDA) Biologics Advisory Committee, a past member of the FDA Science Board, and is a recipient of the FDA’s Cody Medal. He is a past editor of the Journal of Immunotherapy and past president of the Society of Biological Therapy. He has served on the National Cancer Policy Forum of the Institute of Medicine and is a past co-chair of the Cancer Steering Committee of the NIH Foundation Biomarkers Consortium. A past Board Director of the Ontario Institute for Cancer Research, he currently serves as a Board Director for the Multiple Myeloma Research Foundation. He served as Chairperson of the American Association of Cancer Research (AACR) Finance and Audit Committee for 15 years and is a previous elected Board Director of AACR. Dr. Parkinson was a Director of Facet Biotech, Inc., until the acquisition by Abbott Pharmaceuticals, and was a Director of Ambit Biosciences until the acquisition by Daiichi Sankyo. He was also previously a Director at Threshold Pharmaceuticals and Cerulean Pharmaceuticals. He currently serves as Director on the Boards of CTI Biopharma, Inc (CTIC), 3SBio Inc (1530.HK) and is a Co-Founder and Director of Refuge Biotech, Inc. He has held academic positions both at Tufts and at the University of Texas MD Anderson Cancer Center, and has authored over 100 peer-reviewed publications.

Gleevec (Imatinib) is a very effective drug for treating chronic myelogenous leukemia. It acts by binding to and inhibiting the signaling molecule Abl kinase with extreme specificity. Abl kinase is very closely related to Src kinase, and, in fact, the drug binding pocket for Gleevec is almost identical between the two proteins. Interestingly, however, Gleevec binds to Abl 3000 fold more tightly than it does to Src. Why? In her second talk, Kern answers this question. Her lab used NMR, and the techniques she described in Part 1, to show that the protein dynamics of Abl and Src are dramatically different when Gleevec is bound. In a clever experiment in which they synthesized proteins that were likely evolutionary ancestors of Src and Abl, Kern's lab was able to show how changes in amino acids throughout the kinases determined the differential binding affinity of Gleevec for Abl kinase over Src kinase. Experiments such as these demonstrate the importance of understanding protein dynamics at the atomic level of the whole protein, not just the drug binding site, when designing new drugs.

Dr. Hayes interviews Dr. Lippman discuss on being one of the first translational scientists in solid tumors.   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. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. Welcome to JCO's Cancer Stories, The Art of Oncology brought to you by the ASCO Podcast Network, a collection of nine programs covering a range of educational and scientific content and offering enriching insight into the role of cancer care. You can find all of these shows, including this one, at podcast.asco.org. Welcome to Cancer Stories. I'm Dr. Daniel Hayes. I'm a medical oncologist and a translational researcher at the University of Michigan Rogel Cancer Center. I'm also the past president of ASCO. I'm really privileged to be your host for a series of podcast interviews with the founders of our field. In this series of podcasts, I'm hoping I'll bring appreciation of the courage, the vision, and the scientific background among the leaders who founded our field of cancer clinical care over the last 70 years. I think that by understanding the background of how we got to what we now consider normal in oncology, we can work together towards a better future for our patients and their families during and after cancer treatment. Today, I am privileged to have as my guest on this podcast Dr. Marc Lippman. Dr. Lippman was really instrumental in the early studies of the role of the S receptor in breast cancer. And personally, I consider him with his former colleague Dr. William McGuire the first investigators to perform what we now call, quote, "translational," end of quote, science in solid tumors. Dr. Lippman was raised in Brooklyn. He received his undergraduate degree at Cornell where, by the way, he played on the varsity tennis team. And then he got his medical degree at Yale. He did his residency at Johns Hopkins and returned to Yale for a fellowship in endocrinology. Somewhat surprisingly, to me at least, he served a year from 1970 to '71 as a clinical associate in the leukemia service at the National Cancer Institute while simultaneously working in the laboratory of biochemistry with Brad Thompson, with whom he published extensively. Dr. Lippman has authored nearly 500 peer-reviewed papers. He co-edits Diseases of the Breast, which is considered the Bible of breast cancer with Dr. Jay Harris and Monica Morrow and Kent Osborne. And fundamentally, he has mentored the leaders of breast cancer in the world, in my opinion. Welcome to our program. Hello. I have a number of questions I'd like to ask you. First of all, clearly, you took a really unusual path to being a cancer doctor. To my knowledge, you actually never formally trained in oncology. Can you tell our audience how you went from being an endocrinology Fellow to being an oncologist? I think it's worth it, from my vantage point, to give a little background about me. I came from very, very intellectually rich family. And there was never any question that I was going to do some kind of science. I was certain that that's where I was headed. And when I was in medical school, I think it's important that while everybody was doing research at the school like Yale, a lot of medicine as we now think of it as evidence-based was completely mysterious. In those days, when I was starting medical school, really, I think the only fully scientific field was infectious disease because we had Cox postulates. And we knew what drugs killed what bugs. And we knew what bugs caused what diseases, for the most part. And that was wonderful. But endocrinology, at that time, was completely functional assays. It was completely not scientific. You looked to see if the rabbit ovulated or something like that for a bio assays. And Nobel Prize winning research was done, which developed the radio immuno and the radio receptor assay. And that completely transformed endocrinology over night. And within about one year, virtually every endocrine disease, the pathophysiology of Addison's, thyroid disease, you name it was worked out based on being able to measure minuscule amounts of hormones. And to me, this was fabulous. I was going to be an endocrinologist. I had no doubt about it. This was real science. And I could get into it. When I was in medical school, you had to do a thesis. And for reasons that I'm not even sure of now, I can recall, I got involved with a guy who was a hematologist. But he did work on leukemia. And I enjoyed that work greatly. It was very interesting. And right about then, you may recall, there was a minor episode going on called Vietnam. And many physicians or people who were about to become physicians, myself included, weren't very anxious to go to Vietnam. And one of the main alternative routes was to become an officer in the public health service at the NIH and to do your military service at the NIH. And that seemed like exactly what I wanted to do. It was a very unusual process. People at the NIH picked you for their own personal lab. And because I had been working in this hematology lab, a scientist, an administrator actually at the NCI invited me to join his lab, Saul Perry. And I took him up on that because that seemed like my only alternative. But after I finished my internship and residency and showed up at the NIH, because I was part of Saul Perry's group which was the leukemia service, I had to spend a year on the wards taking care of extremely sick people, most of whom died during that year. But because of my love of endocrinology, I kept studying all kinds of stuff around endocrinology, took the molecular endocrinology courses. And then I met this wonderful mentor, Brad Thompson. And my first project with him actually was an attempt to combine leukemia and endocrinology. And I started measuring glucocorticoid receptors in leukemia. And that's, frankly, some of the best work I ever did. We showed that they existed, that they were receptors, and that they predicted response. I mean, we did in leukemia what people were doing in breast cancer, and I thought that was pretty interesting. And there was always this tension in my mind between the science of endocrinology and the almost complete lack thereof, at that time, in oncology. And I thought that I might try to think about putting them together. But I needed to do formal endocrine training. So after I finished my clinical year at the NIH and my two years in the laboratory with Brad Thompson, I went back to Yale to do endocrinology. And I thought that's where I would complete my career. After I'd been there about a year, Paul Carbone called me up and said, would I like to come back to the NCI and join the breast cancer service? And I have to tell you candidly, I had never treated a case in breast cancer in my life when I went to join the breast cancer program at the NCI. And I completely learned everything I learned about breast cancer absolutely on the fly. So what made Dr. Carbone call you to do breast cancer? Well, I'm not absolutely certain. I had done well at the NCI. I'd been very interested in a lot of things. And I'm not certain I can remember anymore. I don't remember why Paul called me, but he did. And at that time, I had been looking at several endocrine jobs at a variety of institutions, including University of Chicago. And I was thinking I'd just spend my life as an endocrinologist. But I thought this was such a great opportunity to pursue my research that I decided to take my chances. I was extremely full of myself in those days. And I didn't see the problem that I had never treated breast cancer. I know it sounds dumb to say it. But I actually said, well, OK, I'll figure this out. How hard can it be? And I guess I didn't find it all that hard. And at that time, because I had already gotten into what I would refer to as molecular endocrinology, half of which was steroid-hormone action, I was highly familiar with the work of Elwood Jensen, who was the real pioneer at that time, one of two actually. So naturally, it made sense to me to take the work I'd already done in glucocorticoid receptors and try to make models in tissue culture for how breast cancer responded to hormones, the kind of thing you would never suggest that a newly minted faculty member try a completely insane project, which I was extremely fortunate that it succeeded. You refer to Elwood Jensen. Tell us more about Dr. Jensen and what he did that got you where you were. Well, Elwood was a tremendous scientist and basically a chemist. And people don't understand how technology sometimes makes a field possible. And just as I mentioned before, radio immuno and radio receptor assay made the entire field of endocrinology and now so many other subspecialties of medicine possible as you measure pulmonary and GI and cardiac hormones, in the same exact sense, what Elwood succeeded in making was radiolabeled steroids. And you can't do receptor assays unless you have high specific activity compounds. We don't use radio isotopes touch so much anymore, and people don't appreciate that. But there was absolutely no way to measure the binding in picomolar and centimolar ranges without high specific activity steroids. And Elwood was able to manufacture created hexestrol, which is a similar compound to estradiol. And with that, he was able to basically separate bounds from free hormone and prove the existence of receptors. It was extremely important studies that he did at the time. And it opened up the entire field of hormone dependency in breast cancer, which, up until that time, had been based entirely on clinical criteria for response. And furthermore, what occurred almost simultaneously with that was finally the invention of some serious drugs that could interfere with hormone action, most notably tamoxifen but several others that were synthesized at the time. And so rather than just having to oblate organs or use very toxic super pharmacological doses of steroids to treat patients with breast cancer, there was now a readily obtainable and usable oral therapy. And so there was a tremendous need to figure out how and why it worked. And a lot of people got into that field relatively rapidly. Bill McGuire being among them. James [? Whitless ?] being among them, myself for sure. And all of us felt that this was an extremely important aspect. There was the clinical aspect, which became clear in the early '70s that there was, as you would expect, a very, very nice correlation between the presence of receptors and response. And that led up to the entire opening of this field of now that you could measure these receptors of how they worked, where they bound, what they did, what genes they induced. And so that became a lifetime exercise for many. My impression is that before about 1970, endocrine therapy, which dated back the 1890s, was mostly done by the surgeons. Did you have to muscle your way into that field? Or were they openly agreeable that some guy who had never even did oncology would start treating breast cancer patients? Well, I think that what was going on then, in England, there was a much greater delay in medical oncology as a field. And these patients were still treated by surgeons and radiation oncologists. I don't think there was any parallel issue in the United States. There were some very wonderful pioneering surgeons, but they didn't, I think, pretend to fundamentally want to get into molecular endocrinology. I don't recall that as being an area of conflict in terms of doing these kinds of studies. And of course, in this country, we were unbelievably blessed by the extraordinary, absolutely extraordinary pioneering and organizational skills of Bernie Fisher, tremendous scientist, in his own right, a tremendous surgeon, but, even more importantly, the ability to really form the most effective, ragtag, co-operative group the NSABP, which was able, from its very inception, to do some of the most groundbreaking studies not just around hormone therapy, which they certainly did, but obviously as we all know about, differences in surgical care. And so-- You eluded to Dr. Carbone. My impression is the NCI, mostly, in those days, was all about leukemia and lymphoma, the so-called gang of five, MOPP and CHOP and Doctors Frei and [INAUDIBLE]. Who was behind you to move out and start taking care of patients with cancer in a more scientific basis? Was it just Carbone or were there other people at the NCI who [INTERPOSING VOICES] Well, shortly after I got, there Paul left. He went to Wisconsin. And Doug Tormey, who had been nominally head of the breast group, departed. And so I was suddenly given an empty stage and said, well, why don't you do it? So within two years, I was running a program in which, the previous year, I hadn't even treated a patient. It was extraordinary. But right about that-- I was-- that's a very good question and a slightly personal one. About 30. About 30, 31. Yeah. Most 30-year-olds now are just starting their residency or their fellowship. Right. And it is unfortunate that people with the most energy and most intelligence get increasingly pushed downstream. I mean, the age of first RO1s in this country is horrible, as we all know. And that's a major other problem that people need to address. But at that time, as you may recall, several groups were developing the first multi drug combinations for breast cancers. CMF, or as Johnny [INAUDIBLE] used to refer to it as CMF, and of course other variations with the MD Anderson regimens of so-called FAC chemotherapy, F-A-C, and other regimens that included vinca and prednisone. And so for the first time, reasonably active regimens were available for metastatic disease. Where in the past, it had only been a handful of single agents, vinca, methotrexate, 5-FU. And at the same time, I think there were the extraordinary, a little bit later, the extraordinary first data that adjuvant therapy was successful. I mean, the studies done by the NSABP initially was single agents and then the CMF studies from Milan were extraordinary. I mean, breast cancer was and remains the most tractable of the solid tumors with the possible exception of testicular that we've treated in this country or anywhere. Tell us about your lab work and how you established what you did, and then really interested in how you looked at what you were doing in the lab and said, jeez, this relates to my clinical work. Well, thank you. As I said, when I had been working at Yale before I came back to the NCI. And at that point, at Yale, I was trying to develop models of gluconeogenesis in liver cells. It had nothing to do with cancer. And so I arrived at the NCI, recruited by Paul, offered some laboratory space, and said, go to it. And I literally, literally scratched my head and said, well, what am I going to do now? And because I hadn't had a previous thing I was just going to expand on. And because another great miracle that had been growing from very late '50s to the mid '60s was cell culture. I don't think people can now imagine how pioneering the results were to grow cancer cells and to get them to reflect, in any sense, the phenotype of human malignancy. I mean, now we take it for granted. But these were pioneers trying to figure out how to grow cells, Harry Eagle and Hamm and Dulbecco, and all of these other wonderful people. So anyway, it seemed to me, wouldn't it be great, since someone had described a cell line that had estrogen receptor, I said to myself, what would be more straightforward than to figure out how you could manipulate these breast cancer cells with hormone therapies and figure out the mechanisms by using cell culture as a model for steroid hormone action? So I set about doing that. And after about six months, I succeeded. And that was the good news. And ironically, the better news was that nobody else could reproduce it, including Dale McGuire. And lots of people said this was, frankly, garbage, that I was making it up. And so when eventually-- no. It was very upsetting. I don't think many people when they first start off and they have their first big set of papers, and I published this stuff in Nature and serious journals. And all of a sudden, everybody says, it's not true. I remember giving a lecture at Harvard. And somebody at the end at the questions said, we just can't reproduce this data. We don't think you're telling the truth. I mean, how often you want to have that happen in your career? And as I said, what turned out to be very fortuitous was that we were right. And so eventually, that made things even easier for me in terms of my career. There's no question about that. And a lot of people wanted to go to the NIH. I think it's now with so many wonderful-- what are there more than three dozen comprehensive cancer centers? But the United States in those days, there were just a handful. And most of them were doing leukemia and lymphoma, like Stanford, which certainly had almost no breast cancer program at the time. And so people who wanted to work in breast cancer came to work with me. And lots of people wanted to get a BTA degree, Been to America. So I was fortunate to have some very outstanding people from Europe and Asia come to participate in my work. And there was still the tail end of Vietnam. So some of the very best and brightest, if I could misuse that expression, people like Neil Rosen and Ed Gellman and Doug Yee and George Wilding, people who all became cancer center directors were people that I was very fortunate to have work with me. And I was pleasured to deal with them. When did you say you were doing the lab models of cell lines and discovering how ER mediated the effects of estrogen? When did you start saying, let's take this over to the clinic? I mean, what was the first thing you did that you translated into the clinic? Well, the first translational study I did when I was a fellow when I tried to do correlations of response to glucocorticoids in leukemic patients and ALL and AML. So I mean, I was used to going back and forth that kind of way. And we did a series of drug trials in breast cancer patients. I was seeing patients. I haven't spoken much about it. But I don't know how to say that any other way whether it sounds modest or not. I simply love being a physician. I found that the main appeal of oncology was dealing with people at times of enormous obvious stress and disturbance in their lives. And I found that that brought out some of my best skill sets. And so I was anxious. I was always involved with patients like that. One of the main trials that we got involved with involved Allen Lichter because Allen and I were endlessly discussing what was the right therapy for localized breast cancer. You may recall that Sam Hellman, the joint center, refused to be part of clinical trials looking at lumpectomy and radiation, as he was convinced, turns out correctly, that that was equivalent to doing mastectomy. And we felt, Allen and I, I think somewhat maybe arrogantly again, that we could do a single institution trial for lumpectomy versus radiation. And we did. We ran a randomized trial of about 350 women at the NCI, a prospective randomized trial of lumpectomy and radiation versus chemotherapy. And of course, all of these patients became fodder for advanced disease trials and everything else we were doing. And those are some of the happiest days of my life working with Alan side by side in what may have been the first multidisciplinary clinic in breast cancer. If I may, I'm going to interject. Allen Lichter, who started the department of radiation oncology at the University of Michigan, where I'm sitting right now, was my dean when I arrived here, became ASCO president at one point, and then was the ASCO CEO for years. Since this is an ASCO publication, if you will, I'd give him credit for all of that. And well he deserves it. Well he deserves it. Yeah. I can't agree more with that. That's for sure. The other thing I've heard you-- by the way, I've always wondered. How did you get 350 patients onto that trial at the NCI, since you've tended not to see walk in the door kind of breast cancer patients, right? So how did you? Well, the NCI remember, everybody was treated free. So fortunately or unfortunately, given American medical economics, people who had a diagnosis would come to see us because they had no other option. We would pay all their travel and everything else. So we treated patients. And I have to tell you, up until last year when she died, I still had patients from that study who had followed me around the country to be treated. That's a great story. It's true. It's absolutely true. So the other thing I've heard you talk about, and I think people should-- given the proliferation of medical journals now, there's one on every corner, I've heard you talk about the fact that you really have a hard time finding places to present your endocrine results, that the Endocrine Society didn't care about cancer. And AACR didn't care about endocrinology. ASCO didn't really exist almost in those days. Give us some stories about that. Well, that's completely true. It's completely true. There was always a session in the Endocrine Society called cancer and hormones, which was late on Friday afternoon. And everybody had gone home. And AACR had the same thing. Because at that time, there just wasn't an obvious niche for cancer. What began to make it more popular to both societies were when things like, quote, "growth factors," close quote, became more in evidence. And they clearly played a role in cancer. But clinical trials and clinical experience had no role in the Endocrine Society. And basically studies in molecular oncology just didn't seem all that attractive to AACR. It wasn't like you couldn't talk about it. It just wasn't front and center what people were interested in. Everything goes through vogues periods. We're now going through an immunooncology voguish period. And I'm not trying to suggest that that's not extremely important and going to have endless value for people. But now, if you're doing almost anything else, you can't even write a protocol. It's true. It's true in some ways. I was trained. [INAUDIBLE], who's an endocrinologist, was at the Dana Farber and told me that cancer is just endocrinology gone wild. In fact, I believe, in many respects, that's what precision medicine is all about is that we begun to take what you guys did 50 years ago and said, let's do it for all the diseases other than immunology, which is a different issue. I agree with you. I think that that's a good point. I think that one of the fundamental differences between normal and cancer, however, is genomic elasticity. If you had psoriasis, and I put you on methotrexate. Then 10 years later, I doubled the dose, it would kill you. Because you never amplify the target gene, dihydrofolate reductase. And you remain sensitive throughout your entire life. Whereas doing that with a leukemic cell, in a couple of months, you'd be completely resistant. And that is, in my mind, one of the shortcomings of so-called precision medicine in which you're trying to match a pathway, an oncogene, to a specific therapy. In that, oftentimes, these studies are in end stage patients with multiple resistant clones now has become endlessly clear from single cell sequencing studies. And I think that there is, I think, personally, slightly less to most efforts in precision medicine than most people think. And I believe that it's amusing that precision medicine has come to include immunooncology, which has little, in my mind, to do with the initial way in which precision medicine was touted, which is find the oncogene. And we will give you the drug. And I think, by and large, that, except for some incredible successes like Gleevec for CML, hasn't really panned out. Personally, I think what we're going to do is head back to what doctors Hall and Frei and [INAUDIBLE] taught us, which is that resistance is a heterogeneous issue, and we need to combine drugs. We just need to do it more thoughtfully than perhaps we've been doing in the past. Couldn't agree more. I want to change the paths for just a moment. To my knowledge, you are one of the few and maybe you were the first oncologist who's been both a cancer center director at Georgetown's Lombardi Cancer Center but also a chair of medicine. You've been at two major academic centers, here at the University of Michigan and University of Miami. Why do you think there have been so few oncologists who have been chiefs of medicine, chairs of medicine? Well, your personal favorite institution, UT Southwestern, would be an example as well of a chair of medicine who's an oncologist. Right. But no particular reason comes to mind. I think that the skill sets and interests of a chair of medicine, at least as it used to be, up until maybe about 10 years ago, were someone who actually wanted to, A, have somewhat less of a research footprint, which would discourage some people, and something less of the same focus on curing a specific disease, which would certainly describe a cancer center director. And I think that exactly explains some of my clinical interest in becoming a chair of medicine at Michigan. I went there, there are always push and pull reasons. The push reasons were that Georgetown was economically a disaster. And they had sold both the hospital and the clinical practice to a large non-profit community-based hospital. And I thought that would be, more or less, the end of the cancer center as I knew it in. And unfortunately, that prediction turned out to be, in many ways, correct. So there was push issues. I just didn't want to officiate over the deconstruction of the cancer center that I had helped to build. And in addition, I felt clinically, I was raised in the era of great chairs of medicine. I was raised in the era of Don Seldon and Dan Foster and A. Magee Harvey, and people who knew everything and would teach at the bedside and knew everything about disease. And frankly, I felt that breast cancer clinically, not emotionally and not from a research point of view, but clinically is relatively straightforward and not that complicated. And I wouldn't say I was bored. But I was looking for a new challenge. And I thought the notion of really trying to bring other areas to bear in terms of my research would be fun. And so I was thrilled to be chair of medicine. But I don't think that's necessarily the career path that many oncologists or any other subspecialist would want. Which did you enjoy most, being cancer center director or being chair of medicine? Unquestionably, being cancer center director here at Georgetown. It was the thrill of a lifetime. When I came here, there were three people in the division of hematology, oncology. Two of them immediately left. And by the time I moved to Michigan, the Department of Oncology that I had created had more faculty than all of the basic science departments at Georgetown combined and more research money than all of the basic science departments at Georgetown combined. It was tremendously happy, very successful. And I felt we were doing really wonderful things. It was just a fantastic time, just like that, which is one of the reasons why I've come back. And I was going to say, although Georgetown did fall on hard times. My opinion is grown back into a major institution. And I'm sure they're happy to have you back. So we're running out of time. I really just touched the surface of many of your contributions. In addition to your scientific contributions, you really touched on it. You've been one of the most prolific mentors in our field in my opinion. I looked over your CV. I count at least six cancer center directors. I think five, four PIs and probably hundreds of others who are proud to have been under your watchful training eye, by the way, including myself, in our careers. So of all the things you've done, your science, your administration, your mentoring, we've touched on all three of those. How do you want people to remember Mark Lippman when it's all said and done? So there's a wonderful joke about that. These three guys are standing around saying what would they like to hear said around their coffin when they're dead. And one guy was a teacher, and he says, you know, I'd like them to remember what a wonderful teacher I was, how I helped people. And another guy's a physician, and I'd like to hear if I'm lying in my coffin, them say, what a wonderful physician. He did everything for his patients. The third guy says, what I'd like to hear is, look, he's moving. So it's hard to-- right. I am certain that the place that I feel most happy, it's not even a close call, is the ability to have played an important role in helping people's careers succeed. I mean, I'm something of a tough guy. But I have been, I feel, very willing to see people grow up and leave the nest and keep them nurtured and look after them for many additional years in their career and enjoy those relationships. It's incredibly enriching. Well, I also have to say there are hundreds of thousands, if not millions of women who have benefited from the contributions you and your colleagues made 50 years ago at the NCI and since then. I've tried to make it clear through all these podcasts how much we owe all of you for what you've done and where we are now. And the reason we're doing this is so people don't forget about those things as we move into medical economics and some of the other things that I think are less fun. So it's time to conclude here. I want to thank you for taking your time. And again, thank you for all you've done for the field, for those of us who've trained with you, and again, mostly for our patients. And I hope you've enjoyed this conversation as much as I have. Very much, Dan. Thanks for including me in this podcast. Until next time, thank you for listening to this JCO's Cancer Stories, The Art of Oncology podcast. If you enjoyed what you heard today, don't forget to give us a rating or a review on Apple Podcasts or wherever you listen. While you're there, be sure to subscribe, so you never miss an episode. JCO's Cancer Stories, The Art of Oncology podcast is just one of ASCO's many podcasts. You can find all the shows at podcast.asco.org.

Brian Druker, M.D., revolutionized the treatment of cancer through research that resulted in the first drug to target the molecular defect of a cancer while leaving healthy cells unharmed. Marketed under the name Gleevec®, his discovery turned a once-fatal cancer, chronic myeloid leukemia, into a manageable condition.  Devin Kelly of Oregon Active & chats with us about the nonprofit. Music licensed from Soundstripe.Support the show (https://www.paypal.me/pdxpod)

In this episode, Siddhartha Mukherjee, oncologist, researcher, and author of the Pulitzer Prize-winning book “The Emperor of All Maladies: A Biography of Cancer,” discusses his writing process, his thoughts about medicine, cancer, immunotherapy, and his recent collaboration on a study combining a ketogenic diet with a drug in mice that provided remarkable and encouraging results. We discuss: Sid’s background [5:00]; How Sid and Peter met [6:00]; Sid’s Pulitzer Prize-winning book: The Emperor of All Maladies [8:00]; Sid’s writing process: the tenets of writing [12:30]; Our struggle to find preventable, human, chemical carcinogens of substantial impact [23:30]; The three laws of medicine — Law #1: A strong intuition is much more powerful than a weak test [26:30]; Law #2 of medicine: “Normals” teach us rules; “outliers” teach us laws [32:00]; Law #3 of medicine: For every perfect medical experiment, there is a perfect human bias [35:00]; The excitement around immunotherapy [38:15]; The story of Gleevec [46:00]; How does the body's metabolic state affect cancer? [49:30]; Can a nutritional state be exploited and/or a drug sensitivity be exploited through a nutritional intervention? [52:00]; How does Sid balance his family, writing, research, laboratory, and patients? [1:00:30]; and More. Learn more at www.PeterAttiaMD.com Connect with Peter on Facebook | Twitter | Instagram.

In the second episode, Ray Futia, Francis Aguisanda, and Paul bump talk about the development of Gleevec: a successful, effective cancer drug born out of decades of basic scientific research and global collaboration.

Deborah Dunsire was a general practitioner in South Africa when a motorcycle drove her into industry. And that side trip, ultimately routing her to Boston, is still going on. She built the North American Oncology unit at Novartis, launched Gleevec, ran Millennium after the millennium, realized the value in Velcade, took a foray into Forum, and recently announced her latest role, President and CEO of XTuit Pharmaceuticals. 

Dr. Ameet Sarpatwari is an epidemiologist in the Division of Pharmacoepidemiology and Pharmacoeconomics at Brigham and Women’s Hospital. Stephen Morrissey, the interviewer, is the Managing Editor of the Journal. A. Sarpatwari, J. Avorn, and A.S. Kesselheim. State Initiatives to Control Medication Costs — Can Transparency Legislation Help? N Engl J Med 2016;374:2301-4.

You'll see more top-selling drugs go generic in 2016. But don't expect drastic price drops initially...the first generic usually has 180-day exclusivity before other generics come out. Prepare patients for these switches. Explain these are best-guess release dates...they can change due to legal maneuverings, etc. OxyContin (oxycodone ER)...available now. But advise patients generics are only out for the 10, 20, 40, and 80 mg tabs so far. Gleevec (imatinib)...February. This could be a game changer for certain leukemias...since the brand costs about $10,000/month. Crestor (rosuvastatin)...May. This is big...it's the only high-intensity statin besides atorvastatin. Consider rosuvastatin if interactions or muscle problems are an issue with atorvastatin. Nuvigil (armodafinil)...June. Explain armodafinil may last longer than modafinil...but there's no proof it's better or safer. Suggest either option for shift workers if nondrug treatments (sleep hygiene, etc) and caffeine aren't enough. Benicar (olmesartan)...October. It will join a handful of other generic ARBs. Pick one based on payer preference. ProAir HFA (albuterol)...December. Explain this generic will NOT be equivalent to Ventolin HFA, Proventil HFA, or ProAir RespiClick. Encourage prescribers to write "albuterol HFA" to give you flexibility. Zetia (ezetimibe)...December or early 2017. Suggest saving ezetimibe as an add-on for high-risk patients who can't tolerate a high-intensity statin. For patients on Vytorin, consider suggesting generic ezetimibe plus a generic statin instead...at least until Vytorin goes generic. Also look for Basaglar in late 2016. It's a new BRAND of insulin glargine that will be similar to Lantus...NOT a generic or biosimilar.