Conversations with the Pioneers of Oncology: Dr. Bruce Chabner
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Dr. Hayes interviews Dr. Bruce Chabner on his experience with cancer drug discovery and development, phase I trials and pharmacology.
Dr. Daniel F. Hayes is the Stuart B. Padnos Professor of Breast Cancer Research at the University of Michigan Rogel Cancer Center. Dr. Hayes\\u2019 research interests are in the field of experimental therapeutics and cancer biomarkers, especially in breast cancer. He has served as chair of the SWOG Breast Cancer Translational Medicine Committee, and he was an inaugural member and chaired the American Society of Clinical Oncology (ASCO) Tumor Marker Guidelines Committee. Dr. Hayes served on the ASCO Board of Directors, and served a 3 year term as President of ASCO from 2016-2018.
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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.
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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 the shows, including this one, at podcast.ASCO.org. Today my guest on this podcast is Dr. Bruce Chabner. Dr. Chabner\'s is widely considered one, or frankly if not the father, of our understanding of the pharmacology principles of anti-neoplastic drugs.
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And probably more importantly, the translation of these principles to the intelligent application of the agents we use in clinic every day. Among the many accomplishments that Dr. Chabner has had working with his mentor, Dr. Joseph Bertino at Yale, who developed the concept of high dose methotrexate leucovorin rescue, that was completely based on their preclinical understandings of the mechanism of action, and more importantly, resistance to this agent. Dr. Chabner was also instrumental in the development of paclitaxel when he was at the National Cancer Institute, and he was intimately involved in many of the early studies that led to better understanding of AIDS and the ways to treat it.
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Dr. Chabner was raised in Shelbyville, Illinois, and I\'m going to digress for a moment, because I\'ve always had a very special soft spot in my own heart for Bruce Chabner. A, because of his science, but more importantly, because I was raised in Shelbyville, Indiana. Both of these towns were named after Colonel Isaac Shelby, who was a hero in both the Revolutionary War and the War of 1812. By the way, Dr. Chabner, I know you were a big student of history when you were in college, so I thought you\'d like this.
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Dr. Shelby became the first and then the fifth governor of Kentucky, and as a citizen he was a land surveyor. There were actually nine counties and 11 cities and towns spread around the Eastern and Midwest regions that are named after Colonel Shelby. And I don\'t know about you, Bruce, but I had this drilled into my brain in eighth grade history class. I had to learn all about Colonel Shelby.
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Anyway, so he and I are brothers in Shelbyville. Dr. Chabner received his undergraduate degree of Yale, where again, he spent a lot of his time in the history department but also in the biology department. And then he got his medical degree at Harvard, where he stayed to complete his residency in internal medicine at the Peter Bent Brigham Hospital before it became the Brigham Women\'s Hospital.
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In 1967, Dr. Chabner became a clinical associate in medical oncology at the National Cancer Institute, where he was, in succession, a senior investigator in the laboratory of clinical pharmacology, chief of the clinical branch of the clinical oncology program, associate director of the clinical oncology program, and then he succeeded Dr. Ben\\xa0[? Stabida, ?]\\xa0someone I have previously interviewed for this series, as director of the division of cancer therapy.
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In 1995, after 25 years at the NCI, he moved to Boston as the chief of the division of hematology oncology and the clinical director of the Massachusetts General Hospital Center, where he is now the clinical director emeritus. Dr. Chabner has authored, I counted, over 500 peer reviewed papers. I think even more than that. By the way, his first was in 1969, a case report of shaking chills related to occult lymphoma, authored with Drs. DeVita and the\\xa0[INAUDIBLE]\\xa0of the\\xa0[INAUDIBLE]\\xa0syndrome. Bruce, that really shows how old you are.
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He\'s been the editor of all five editions of the Principles and Practice of Cancer Chemotherapy and Biologic Response Modifiers, which I consider the bible of cancer pharmacology. And I\'m looking at my fifth edition on my bookshelf right now. He\'s trained too many Fellows for me to name, but numerous of them have gone on to be cancer center directors, chiefs of division, department chairs, and other leaders of oncology in the world. He\'s won way too many awards me to go through, but he received a Karnofsky award from ASCO, and he served on the ASCO board of directors.
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Dr. Chabner, welcome to our program.
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Nice, that\'s a lot of history. It speaks to my name.
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Well, that\'s the problem of interviewing all of you folks. It takes a long time to get through all the things you\'ve done. It\'s a good problem to have, though. First, I want to start out, I understand you carry the flag rank of rear admiral. And I want to know, have you ever even been on a ship? And more importantly, did you and Dr. Shelby actually serve together in the Revolutionary War? I couldn\'t figure that out.
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You know, I never bumped into him when I was on the battleship Shelbyville, but who knows. He seemed to be what I call a name dropper. He left his name on so many different things, and I think there\'s a Shelby County, Tennessee, which is Memphis. Plus I think the smallest thing that he ever created was Shelbyville, Illinois, which was even smaller than your hometown.
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Yep, that\'s true. All right, that\'s the last joke I\'m going to tell in this interview, but I like that connection. Anyway, so how did a guy from Shelbyville, Illinois get to Yale and then Harvard and NCI? And more importantly, what made you decide to be an oncologist? I know your father was a general practitioner, but at that time the field barely existed. What was your motivation?
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Well, OK, I\'ll tell you a bit of a story. My mother came from Chicago and she had a brother who was pretty smart. And he went to Harvard. And he used to come down to Shelbyville because he liked the pies that she made. And we were 200 miles south, so it was a trip for a pie, but anyway we used to play chess together. And when he was a college student and I was like in fourth grade, I beat him in chess and he said, Jesus, you ought to go to an Ivy League school. So that put the idea in my mind.
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And then my parents were not really happy with that. They wanted me to go to Washington University or University of Illinois, but I wanted to get away from home. It was a little bit confining to be around my parents for the rest of my life. So I applied to Yale, Harvard, and Princeton, and the deal was I could go to school if I got a scholarship. So I got a scholarship to Yale, so I went there. I was happy with that choice. I really-- it was sort of, you know, life changing, actually. Stayed on the east coast.
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But I still have many good friends from my Shelbyville days. We all get together once a year to play golf and poker and tell life stories.
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So I have to interject. My father told me I could go to any college in the United States as long as the tuition was the same as in-state tuition of Indiana University, which at the time was $400 a year. So I ended up going to Indiana University. So how did you--
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That was such a great deal. Yeah, that was my--
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How did you get into oncology?
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Well, when I was at the Brigham, I got interested in cancer. There was not much going on there, but one of my residents was a guy named Jack\\xa0[? Moxley, ?]\\xa0who had been a part of the initial study with DeVita and others, George\\xa0[? Kinellas, ?]\\xa0of the mop treatment for Hodgkin\'s disease. And I got really interested in that. And actually during my internship my sister got an immediate stromal tumor during her pregnancy, and it turned out to be a thymoma. But cancer really intrigued me at that point.
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And we all had to apply for positions at NIH as a way to get out of the draft, and I wanted to do research, so that really appealed to me. And I actually applied for cardiology and cancer, and I was interviewed by Gene Brown for cardiology, and he didn\'t seem very impressed. But the cancer people did like me, particularly George and Vince, who had come back there. And they were young and energetic and they had interesting ideas about combination therapy, so I ended up in oncology.
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Yeah, I talked with some of the other people I\'ve interviewed about the so-called era of the yellow berets and how that really transformed medicine, in my opinion. Because so many smart people went to the NIH to stay out of Vietnam. It\'s probably the only good thing that came out the Vietnamese war, as far as I can see, and especially the NCI. So when you went to the NCI,\\xa0[? Harlan ?]\\xa0and Frye and\\xa0[? Freirach, ?]\\xa0I believe, were gone. So you\'ve already started to say, it sounds like Dr. DeVita and Dr.\\xa0[? Kinellas ?]\\xa0were the movers and shakers at the time. Is that fair, or?
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Yeah, well they were really young. I mean, it was like working for, you know, contemporaries. There were no old people there. And Frye and\\xa0[? Freirach ?]\\xa0weren\'t that old at that time. They were in their 40s with Vince and George, who were in their mid 30s. And I was 28 years old, I guess, when I went down there. I loved it. We had laboratory opportunities, we had patients, we had people that believed that they could change the way cancer was treated. George and Vince, particularly Vince, were so energetic and so committed to the idea of changing therapy, and particularly combination therapy.
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And then the other thing that made it such a great experience were the colleagues that I had in my first group of clinical Fellows. Bob Young was part of it, and I became very close friends with Bob Young. And in the same group, David Livingston was my next door neighbor, and we had interned together and been arrested together. So we had just constant stimulation from a lot of different people, all of them energetic and interested in research.
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Who else was in your class besides Dr. Livingston and Young, then?
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Phil Shine, who made a name for himself in toxicology and then in industry. And let\'s see--
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He was director at the cancer center at Georgetown for a while.
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Georgetown, right. Subsequently, there was just a long list of wonderful Fellows. When I came back, I actually spent two years at Yale between my NCI time and then coming back to NCI. And I had a wonderful time with Joe Bertino. He was, I think, very important to me, because he was really a great scientist. And I learned a lot about biochemistry enzyme purification and working in the lab.
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And so when I came back to NCI I had sort of converted to being an anti-folate person from being interested in alkylating agents. And so I was always interested, I guess, in anti-metabolites. But that was a great anti-folate experience with Joe, high dose methotrexate. It was really his idea, not mine. But the thing I worked on was the clinical pharmacology and trying to figure out why it was so toxic to kidneys. So we actually did some really interesting experiments.
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We gave high dose methotrexate to monkeys, and then when they died, we took the kidneys out and looked at them. And we were doing it because we thought we would see interesting pathology. What we saw were a bunch of yellow gravel in their tubules. And it turned out it was methotrexate, and it became obvious what was happening. The drug was precipitating in the acid urine environment. But that was sort of the beginning of the methotrexate studies.
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And personally, I don\'t think we teach pharmacology very well anymore. What made you want to go to high dose methotrexate?
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Well, interestingly, I was particularly interested in-- Joe was trying head and neck cancer. There was almost simultaneously an article from Frye and Isaac\\xa0[? Jurassi ?]\\xa0about adjuvant therapy of osteogenic sarcoma. And there were several interesting things about that. One is that it turned out that 12 patients weren\'t all patients with osteogenic sarcoma. But prognosis of those patients wasn\'t apparently obvious.
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But there seemed to be some success with it, and there was a lot of toxicity that they didn\'t really know how to deal with. And so I started doing pharmacokinetic monitoring in patients that we had that were on the treatment. And then when they went into renal failure, they just didn\'t clear the drug. The drug was hanging around for many days and they were getting this horrible toxicity. So we got into this business of why the renal toxicity and the need for hydration and alkylization, particularly.
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And so first of all, I have to tell you I blamed you for much of my first year as a Fellow, because we had to draw the blood. So there were no study coordinators. Dr. Frye would just run around at all times of day and night drawing blood on patients for getting high dose methotrexate. And I still mumble under my breath when I hear your name.
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Well, you don\'t have to do all of that now, but you know, in those days we were trying to get a more complete profile, so we did. There was a woman there at the Farber that was doing similar work. I can\'t remember her name.
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Sue Pittman I think, right?
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Yeah, Sue Pittman. That\'s right, that\'s right, that\'s right. But that was certainly the introduction to the anti-folate. And then I got into a very interesting area of polyglutamation and how it changed the potency of the drug and led to retention, and it was an important determinant of response. That was quite an interesting area of research.
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Were you the first to report amplification of DHFR? No, that happened in 1978. I was working on MTX at the time and we had noticed that you could select highly resistant cells in culture. But then we were interested in knowing why, and Joe and Joe Bertino had described the fact that increased dihydrofolate reductase activity was found in this circumstance. But the actual demonstration of amplification in mammalian cells was done by Bob\\xa0[? Shimke ?]\\xa0when Joe was on a sabbatical with him.
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And they had a medical student working in the lab on that on that paper, and that was Dan\\xa0[? Haber ?]\\xa0actually. Who came back to--
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Who is now the cancer center director\\xa0[INAUDIBLE], right?
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Yeah, he wrote a key paper. So we had, at the time when that came out, we got interested in that. And we stuck radiolabeled methotrexate in the culture with some tumor cells and found these odd migrating entities that turned out to be polyglutamate. So that led to the whole issue of what were polyglutamates and how did they change the biochemistry? And that was quite interesting, and then actually at the same time we saw a patient.
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It was a young man who came to NIH with non-Hodgkin\'s lymphoma and was treated with high dose methotrexate. I can\'t remember. I think he had CNS involvement or something like this. We found evidence of gene amplification in this patient. So it was actually the first demonstration that gene amplification occurs in people on the drug. There are a lot of interesting things that were happening at that time.
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How was translational medicine before it was called translational medicine?
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That was the nice part of NIH, you know? The emphasis was on the labs working with the clinics, and particularly with physician scientists. So, you know, we were one of the few places where our Fellows were expected to work in labs in their second and third years, and they did, and we had a wonderful group of Fellows that came through. The first guy that worked on polyglutamation of MTX was Rich\\xa0[? Shilske. ?]
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Who is now the chief medical officer of ASCO, and many, many other accomplishments after that.
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Right. But many--
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Actually, I\'d like to change gears for a minute, because I know you had a lot to do with the development of paclitaxel. And I always found that story interesting that, you know, it was in the bark of the Japanese yew tree, which had to do with ultimate supplies. But also the first phase one trials, which some of that was done at the Dana Farber when I was there. Can you just walk through the history of paclitaxel? I think our listeners would love to hear this.
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Well, it was an accident of history. Believe me. The thing started in 1964, when a group at the research triangle, a chemist, isolated this compound from the yew tree. And they didn\'t actually know what it was, but it was cytotoxic. And it was an anti-mitotic, and it took him seven years to figure out the structure. So finally in 1971 a guy named Ronnie from that group published the structure. It was a ridiculously complicated structure, And nobody could synthesize it, at least at that point.
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It hung around in the lab and nobody was interested in developing it, because it was such an odd molecule. It was insoluble. Nobody can put it in solution. So it really wasn\'t an attractive pharmaceutical. And the thing that happened was, in 1978 or 1979, we had a very hot drug that was called maitansine. And we were very eager to put this into the clinic. And it was an anti-mitotic also, and very, very potent drug.
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And so Dr. DeVita asked me to personally shepherd this thing and he told me that he didn\'t want it to fail. And so I put it into patients and it was terrible. And I kept telling him, this is not going to work. He said, it\'s got to work. He was pretty persistent. Well, it didn\'t, and he was very disappointed. So was I. And the fact is, we had nothing else to put in the clinic at that time except for paclitaxel. So we said, oh, well, we\'ll try it.
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And we put it in a lipid emulsion. It was like putting it in engine oil or something, but it went into the clinic in several places. Peter\\xa0[? Wernick ?]\\xa0did it. Einstein. I guess you guys did it at the Farber. And it was causing all sorts of hypersensitivity responses. It looked impossible. And it took about, I don\'t know, four or five years to get it into a regimen that was tolerable. And there had been responses. The first response was in melanoma, so we were all excited about that.
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That was the usual circumstance in those days that, when you took a drug into the clinic, melanoma would be the first response. And no one else from melanoma. Everywhere was-- and so but then Peter began noticing responses in ovarian cancer. And a regimen was worked out with antihistamines so it was reasonably tolerable. And finally in 1991, which was eight years after it went into the clinic, we finally decided, well, it was time to license it to industry. There was no patent, but we did it under a co-operative research and development agreement.
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And the only company that was interested in the US was Bristol-Myers. Everybody else said, this is ridiculous. Nobody wants this drug. And it was too hard to make it. You had to make it from the bark of plants and it was insoluble and it caused hypersensitivity. So they took it. And about a month afterward there was a report from M.D. Anderson saying that it was active in breast cancer. And at that point it just took off like a rocket. And, you know, tried in all sorts of different diseases. Was active in lung and bladder and-- I can\'t remember all the other things. Head and neck.
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Anyway, it became the first billion dollar drug in the cancer drug industry. And I think, you know, there are two things that really set off industry to be interested in cancer. One was that, the fact that you could actually make money on it. And the second was the notion of targeted therapies, which was growing at that time.
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So to my knowledge, this is the only time somebody at the NCI had to work with the US Forest Service and the Bureau of Land Management regarding a new drug. Can you tell that story?
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Well, yes. The only place where you get the raw material for the drug was from the US Forest Service. And so Texas plants were being sort of cut and burned because they were considered scrub and not worth anything as lumber. So they were cooperating. And finally when we licensed it, Senator Ron Wyden, who\'s still in the Senate from Oregon, got interested in this whole thing. He said, why isn\'t the government making money on this license? Why did you license it to Bristol-Myers and you didn\'t you didn\'t ask for anything back?
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And we said, well, you know, that\'s not the function of NIH. We didn\'t have a patent. I guess we could have asked for a slice of the pie, but we didn\'t because no one else wanted it. We really were trying to give it away. And he was giving us a really hard time at this hearing. And then the key thing that happened was a woman who was a forest ranger with ovarian cancer, we found this woman, and she testified to how much good it did for her. And that sort of stopped all the fuss about the license.
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And we actually, it was the first drug where as part of the licensing agreement we had the chance to fix the price or agree to the price that Bristol-Myers fixed. And the government never has done that since that time. Of course, this was a circumstance where we sort of owned the information, so they had to listen to it. But they set the price at $2,000 a course. And we consider that pretty high, but it was sort of equivalent to what other drugs were costing at the time, so we let that go by. But ever since then, the price of drugs has just escalated remarkably.
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I hope there are some young people listening, because this story, in my opinion, the story of trastuzumab again, I think people think that these things just happen because the system makes them. And my experience is they happen because the drug or the treatment gets a hero, gets a champion. Ultimately the science has to prove it works, but I\'m sure lots of people wanted to walk from Taxol.
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You know, everybody thought it was a dog. Because it was, you know, caused hypersensitivity, it wasn\'t all that active in the initial testing, and it was really hard to make the stuff.
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Well, the same thing is true with platinum I did my residency at UT Southwestern with Donald Sullivan, who\'s the chair of medicine. He was a renal guy, and a patient with metastatic-- and I had gone to Indiana. So Dr.\\xa0[? Einhardt ?]\\xa0taught me how to give it. So I had a patient come in with widespread testicular cancer, I wanted to give him cisplatin, and Dr. Sullivan wouldn\'t let me do it because it would hurt his kidneys. I said, Dr. Sullivan, he\'s going to die if we don\'t do this. And he said, he\'ll die anyway.
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And so I did it behind Dr. Sullivan\'s back and I got a complete response. Fortunately in those days the residents didn\'t have a lot of oversight so I could do what I wanted to do. There were a lot of people that thought these drugs should be shut down, and it took the courage that you guys had back at the NCI and other places to push them out.
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Don Sullivan was very anti cancer chemotherapy for the rest of his life. And it was odd for me, because I actually had a relative who was on his faculty and I went down there a couple times to talk. And I always felt very uncomfortable telling him that we were accomplishing something. Because his concept of success in science was getting an RO1 in your lab.
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Yeah. He finally came to terms because\\xa0[? Shelfke, ?]\\xa0myself, Fred\\xa0[? Lemaitre, ?]\\xa0and a number of us went into oncology and had been reasonably successful. And I think he decided that it was worthwhile after all. But it wasn\'t easy for him. We lost him a year ago. I still miss him.
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Yeah, he was an amazing guy, but he really did have a hard time believing in cancer.
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So the other question, I wanted to change gears a little bit, because I know just about the time you became the director of the DCT was when the AIDS epidemic was exploding in the early 1980s. That must have been a very confusing situation about who should be in charge of this at the NIH, which institute, and how you approach it. Can you give us some background on that?
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Again, it was really a crazy time. Because I remember one of the first patients that was identified as having AIDS was a person admitted to the immunology branch at the NCI. Not the medicine branch or the clinical branches. It was a patient who had disseminated tuberculosis and it had no CD4 cells. And, you know, everybody said, oh my god, what is this? This is really a weird, weird circumstance. And then other people began reporting this from San Francisco and New York.
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So we actually, DCT, the reason we got involved was because of Bob Gallo. Bob Gallo had discovered the HTLV1 virus, which was causing this lymphoma in T cells. And we suspected that this might be a syndrome caused by a T cell virus. So in 1981, really quite early, we convened I think the first meeting about the biology of what was called HTLV2, I think, at the time, or three. I can\'t remember which one it was. But at any rate, there were a cadre of people at NIH that felt that it was caused by inhaling gases or, I don\'t know, their various weird theories about it.
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But this theory that made sense to us was that it was caused by a virus. So Sam\\xa0[? Brodeur ?]\\xa0was collecting samples from patients and brought them over to Gallo\'s lab. And of course Gallo mixed those samples with the French sample and found virus and then made a test kit for the virus, which was really a key event in beginning to control the epidemic. And because of all that work going on at NCI at the time, we were asked-- we had the only drug development system at NIH.
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We were asked to, well, look, can you set up a drug development system for this? And Sam\\xa0[? Brodeur ?]\\xa0set up assays in infected T cells and showed that certain nucleocyte analogs could stop the virus from replicating. The first one was ADT. And his first study was, I think, was 16 patients with AIDS in which he showed that the T cell counts recovered and people didn\'t die. And from that point on, we were getting significant funding for doing research on treatment development. And it was it was done in conjunction with NIAID and Tony Fauci.
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What Tony did is he delegated a fellow to work with us and sort of be the liaison. And the first fellow that did that was Margaret Hamburger, who became\\xa0[INAUDIBLE]\\xa0FDA subsequently. And, you know, subsequently, four other people from our division-- well, actually one from NGH, became directors of FDA. Ned Sharpless most recently, and then Steve Hahn, who was a Fellow in the medical oncology group at NCI.
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Yeah, he\'s just been named.
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It was, you know, an unusual breeding ground for people interested in therapeutics.
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That\'s interesting. You know, I was a third year resident at UT Southwestern. I was at the VA in March and a young man was admitted to our service. He had been a Vietnam veteran and he had red splotches all over him, so I called a dermatologist who biopsied it. And I got a page from the pathologist and I called him back and he said, you have mislabeled the samples. And I said, what do you mean? He said, well, this says it\'s a 37-year-old man. This is something I\'ve never seen before, but I looked it up and it\'s called Kaposi sarcoma, and that only happens in old men or people from Africa.
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And I said, I don\'t think we mislabeled things. And I think he was probably the first man in Dallas to be diagnosed with this. Because just as the MWR and the new journal paper came out a few months after that. So again, for the young folks listening to this, and we\'ve already hit this a couple of times, it\'s one or two patients that pique your interest that often change the world in terms of, gee, I wonder why that happened.
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Yeah, absolutely. I mean, you know, a lot of this is an outcome of the fact that you have research people as physicians who are working with patients, and then they ask questions.
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Yeah. One of the things I\'ve carried forward, Dr. Frye used to always say, think like a scientist. Think like a doctor. And ask yourself, so what? And I know you do that, because again, you\'ve already told us today and I\'ve seen you do that in other places. You know, so what? Why did this happen to this patient?
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Why did that happen, yeah.
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What in my lab actually will change that? And you guys did that in spades, I think, 40, 50 years ago. It\'s pretty amazing.
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Yeah. Well, I\\xa0[INAUDIBLE].
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[INAUDIBLE]. Go ahead. Go ahead.
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No, it\'s really happening a lot now, you know, in terms of recognizing subsets of diseases. We used to think that non-small cell lung cancer was just one disease. Now it\'s 20 diseases. It\'s amazing, you know? It\'s amazing, you know, as science progresses, you begin to understand the complexity of cancer. And then therapies become meaningful.
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Yes, I agree.
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It\'s so nice. And so I wish, you know, we were curing people. But we are making a difference, and least we\'re understanding it a little.
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I agree. Anyone who has not heard or read Bruce Johnston\'s ASCO presidential address should do so. Because he did point out exactly what you just said. He had a pie chart, and 10 years ago the entire pie chart was chemotherapy for metastatic non-small cell lung cancer with little or no success. And now the pie chart is well over half the patients getting some kind of targeted or immunotherapy. Yeah, it\'s pretty amazing.
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It is quite\\xa0[INAUDIBLE]\\xa0for young people that are listening to this, is that there are enormous opportunities for doing even better than we did. So we just made a start in this whole thing.
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OK. With that inspiring message, which I\'m glad you said it, we\'ve run out of time. Actually we come at the end of our time. But Dr. Chabner, I want to thank you on behalf of all of us who trained after you, who\'ve learned so much from what you\'ve done, and more importantly, the patients who have benefited from the stuff that you\'ve contributed to the field. It\'s pretty remarkable and inspiring. I don\'t use that word too often, but it is. So thank you, and thank you for taking time today. I hope folks listen to this and say, I\'m going to go back and make a difference here.
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Thank you, Dan. I have enjoyed it. It\'s been a wonderful time in this career.
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Yeah. Well, my pleasure. Until next time, thank you for listening to this JCO\'s Cancer Story, the Art of Oncology Podcast. If you enjoyed what you heard today, don\'t forget to give us a rating or 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.
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