Dr. Larry Einhorn, professor of hematology/oncology at Indiana University, joins The Uromigos to discuss spectacular advances in testis cancer treatments, including his experience in experimental therapeutics.
Episode Transcript
Tom:
Hello, everybody. We are joined here on our legend series by Larry Einhorn. Larry, I’m going to ask you to introduce yourself, but firstly, I’m going to say thank you because we did this podcast a week ago. I thought it was fantastic. Brian thought it was fantastic.
Brian:
Amazing.
Tom:
It was the first one we’ve ever lost. So, I feel terrible on the one hand and we’re really grateful you’re here today. We’ll try and go over some of that ground again because it was so cool. Brian, do you want to start with the first question?
Brian:
Sure. Larry, thanks again for joining us in …
Tom:
Oh, Larry, introduce yourself. Sorry Larry. Sorry. Yeah, introduce yourself Larry.
Larry Einhorn:
Yes, I’m Larry Einhorn. I’m a professor of hematology, oncology here at Indiana University where I’ve been here since 1973.
Brian:
Awesome. So, Larry, take us back to sort of the early days, both of your career in oncology because as I understand it, when you started medical oncology was a new subspecialty. So, I think it’d be interesting to talk about what it was like then, what was ASCO like then, what were the early days of sort of grinding through chemotherapy combos?
Larry Einhorn:
Sure. So, I did a one-year fellowship back when that was all you needed at MD Anderson in Houston and J. Freireich was a mentor to me and a friend to me and his concept of experimental therapeutics, as opposed to just doing the same old 5-FU in colon cancer for example, really created the impetus for my wanting to do experimental therapeutics as well.
And when I joined the faculty here in 1973, there was still the concept that it was okay to treat aggressively for hematologic malignancies, but not for solid tumors where you would just a one long reduction and maybe a two-month partial remission and testis cancer changed that completely. And then those early days, in the 1970s, we didn’t have 30,000 people at ASCO. We were lucky to have 300 people at ASCO.
It was done at a hotel and the hotel, when I did my PLEN recession paper in 1976, was in Toronto. I don’t even think we’ve had any meeting outside the United States for ASCO since. They were in the hotel circles in San Diego, and they were in the hotel in Houston in the early days of ASCO.
And so, when I joined the faculty at Indiana University, we had two classical hematologists on faculty, Dr. Rowan and Dr. Bond, who were both brilliant and they welcomed me with open arms because they were not really geared to doing solid tumor chemotherapy. And I wanted to be looking at diseases that, even back then, were known to be chemo sensitive, not just leukemia and lymphoma, obviously.
And that included small cell lung cancer and of course, testis cancer. And I was very fortunate in my career because when I came here, at Indiana University, we already had a world-famous urologist, Dr. John Donohue, who was chief of the Urology Program here and he welcomed me with open arms.
He was actually giving his own chemotherapy to patients with actinomycin D, an older drug that was used at that time, because he didn’t want to abandon patients after he did these aggressive retroperitoneal lymph node dissections and several months later, they would come back with pulmonary metastatic disease.
So, he was delighted to have a partner rather than doing his own chemotherapy at that time. So, these were very different times. The number of drugs that we used for cancer, other than hormonal therapy and breast and prostate, were all chemotherapy. Immunotherapy didn’t exist. Molecular targeted agents didn’t exist.
Well, maybe interferon to a minor degree. And there was a very small [inaudible 00:04:04] to learn from. And when I sort of … Lucy mentioned that I did a one-year oncology fellowship. That was … If you’re not in the lab, that was all you really needed.
Tom:
Larry, tell me, so cisplatin changed testis cancer. When did you discover that cisplatin was changing testis cancer and you gave a great story last time about how you found out about getting your ASCO talk and then the uncertainty, when you arrived, about durability of responses.
Could you just talk to me about when you saw these tumors melting away. When that first happened and when you realized it wasn’t just going to be a quick response and a relapse?
Larry Einhorn:
Sure. So, when I was at MD Anderson, Dr. Mel Samuels, in a different department; medicine, not experimental therapeutics, was studying high dosages of vinblastine plus bleomycin as a two-drug synergistic regimen. And platinum had interesting studies that were done as a single agent, no durable responses, but definitely showing single agent activity in people who had failed actinomycin D or other similar therapies.
So, because platinum was non mild suppressive, was unique mechanism of cytotoxicity, and was synergistic with vincas like vinblastine and so many other drugs, it felt to be a very simple logical phase 2 study to do. And so, I simply combined cisplatin with vinblastine plus bleomycin.
And because we had the ability to have patients with metastatic testis cancer, because of John Donahue being here, we were able to do a 20-patient study, which actually was first presented at an American Urological Association meeting in Indianapolis.
And then we really started getting patients sent to us at that time and so, when I submitted an ASCO abstract with cisplatin, vinblastine, bleomycin as a phase 2 study, we had 47 patients on it at that time. None of them had more than an 18 month follow up and back then there were no computers.
You would send a little postcard with the abstract and you would have a little box to check about whether you wanted it to be an oral presentation or a poster. You got to choose which one you want.
And so, the abstract was sent together a self-addressed stamp postcard to send back to me. And I get this postcard back saying, “accepted.” I said, “that’s nice.” And then it said, “plenary session.” I had no idea what a plenary session is.
Tom:
Brian still doesn’t by the way.
Larry Einhorn:
I had to look up the word plenary session. So, I was getting a little diaphoretic at that time because the nature of my studies in small cell lung cancer is they would get these great remissions and six months later, they all progressed with extensive small cell lung cancer.
And I felt I was going to look foolish being on a plenary session, talking about these nice remissions and “oh, by the way, between December and June abstract submission and presentation, these patients all relapsed.” And so, it didn’t really matter that much.
Tom:
Larry, I have two questions. One: Do you still have that post part you’d like to put in the Ecology Hall of Fame somewhere and was there a day … I mean, I’ve had the experience where you’re looking at scans … For me sort of early days of sunitinib or something where you’re looking at scans and you’re thinking, gosh, this drug really works or something.
Was there a day, or a place, or a patient, where it was sort of that eureka moment with platinum and testicular cancer?
Larry Einhorn:
Well, you guys can probably remember when you were starting out also, we were all young and dumb. We thought everything was going to work. It was a golden era. We had these new experimental drugs, doxorubicin, the nitrosoureas, platinum and many other drugs coming out on the market at that time.
So, the very first patient to get platinum, vinblastine, bleomycin, was a patient who’s a schoolteacher in Indianapolis by the name of John Cleveland. And he’s really a hero to the testicular cancer population, because he received this as third or maybe even fourth line therapy. He knew that platinum caused horrendous nausea and vomiting, because that was known from the earlier single agent studies with platinum.
He had no idea whether this would make him live one day longer and yet he was willing, and we had no effective ANI medics back then.
And he was willing to go through these 5 days of therapy and come back 3, 6 and 9 weeks later for a second, third and fourth course. So, we had refractory disease with growing pulmonary metastases and rising HCG levels. And after the first course, his tumors completely disappeared. His hCG normalized. And we thought that was great.
That was one of the postcard patients. But once he was out at a year and remaining continuously disease free, because most of the actinomycin D or vinblastine, bleomycin complete remissions, when they relapsed, relapsed during that first year. So at least we had an in of one with our first patient to know that some patients would have durable remissions.
And I think when we look at how we define complete remission back in the 1970s, we were able to define it, of course not just with imaging studies, but also with a serological quintessential biomarker with hCG and alpha fetoprotein levels.
And so, we probably had a little better definition, biologically, at what a CR was as opposed to what a PR was and other types of tumors. So, I think the eureka moment was really when we had about a half a dozen of these patients, all who are remaining disease free, all beyond one year, that we realized that this really was a major advance in that it was my walk on the moon, so to speak.
Our famous patient, Lance Armstrong, but Neil Armstrong with the walk on the moon, you do this once in your career. And it made just a monumental difference. And when I give lectures to not just oncologists, but to non-oncologists, I make the point that, when we started these platinum studies with testis cancer, it had been used at other institutions as a phase 1 drug in many different diseases: colon cancer, melanoma, pancreatic cancer, with very minimal activity.
And just as platinum has saved the lives of thousands, tens of thousands, probably hundreds of thousands of young men over these 40 plus years, testis cancer saved platinum. Because at the early phase 1 meeting that I attend through the NCI, when they look at the new experimental drugs, a comment was made that if we’re presenting platinum, as one of them, we have a real problem in our field because it has such a bad reputation with toxicity and very minimal activity.
But if a drug works, the oncology community will figure out how to mitigate the side effects, which have been largely done with cisplatin. I really do think, if there were no such disease as testis cancer, there would be no such drug as platinum, based upon those earlier studies in the 1970s with the far less responsive tumors.
Tom:
Larry, why is cisplatin better than carboplatin in testis cancer where that’s not the case in lung cancer?
Larry Einhorn:
Yeah. And certainly, in ovarian cancer is a dead solid even break. There’s no difference at all. In lung cancer, you have to do a meta-analysis to show a very minor difference, measured in weeks, favoring cisplatin over carboplatin, which is why our adjuvant trials, incurable lung cancer, used cisplatin instead of carboplatin.
But there’s no question from randomized studies. As you well know, there are two of them on both sides of the Atlantic Ocean that showed a superiority of cisplatin over carboplatin. I worry a little bit about the studies that are done by our pediatric colleagues, which are, once again, looking at carboplatin as first line therapy.
And in my rather limited knowledge of pediatric oncology, because I don’t treat patients under the age of 13, I think the pre-pubescent young men do just as well with carboplatin as they do with cisplatin. But once you’re over age 13 and you’re post puberty, I think it’s questionable whether carboplatin is a drug that should be used compared to cisplatin, knowing that the toxicity is less with carbo than with cis.
Tom:
Larry, where are the areas in testis cancer since those early days of your triplet, perhaps cisplatin placed treatment, what are the subsequent areas of progress that have been made in testis cancer?
Larry Einhorn:
Well, there’s been a lot and just starting out with drug development, etoposide came around in the late 1970s, and we and others looked at that as single agent therapy and people who were not cured with PVB, it produced responses, but no cures. And then we found from work with Dr. Skipper and Dr. Shapiro in Birmingham, Alabama, that the most synergistic combinations with platinum were platinum plus fluorinated parametings, 5-FU and also etoposide.
And so, we did a study of cisplatin, etoposide as second line therapy curing 25% of the patients. And that’s the first time it was a curable disease as second line therapy. And as you know, BEP then replaced PVB. And I think advances have been made over the decades. We do much better with antiemetics and supportive care, which is so important for quality of life of patients that used to suffer through the terrible nausea and vomiting.
We have an experimental marker with the microRNA 371, which is still experimental. It’s not going to replace hCG and AFP, but it looks like it could be a nice compliment to hCG and AFP in making decisions and the design of clinical trials and testis cancer, we become a victim of our own success.
So, 60% of patients who get chemotherapy for testis cancer have what’s called good risk metastatic disease. And when you’re dealing with over a 90% cure rate in those patients, there probably are few, if any, rational clinical trials that can be done showing that you can do better than that or even to show a non-inferiority study with a shorter duration of therapy, as we once did with four courses versus three courses.
Tom:
Larry, you once showed … You had a new journal cisplatin, etoposide, high dose. So, you’ve got high dose therapy and of course there is TIP, which is also widely given as in … This is platinum refractory, urothelial cancer relapse. I’m sorry. Testis cancer. Relapse test is cancer. Cisplatin, etoposide, high dose.
You published that in the New England Journal of Medicine. Many people around the world are giving TIP as second line therapy or VIP.
Larry Einhorn:
Right.
Tom:
What is your take on the second line space and how you think we should proceed?
Larry Einhorn:
Sure. And it’s really hard to do randomized studies and Darren Feldman, at Memorial Sloan Kettering, and York Byron, in Europe, have designed the TIGER trial, which is going to hopefully answer that question of second line therapy. And the study designed is to use standard dose chemotherapy with Taxol, ifosfamide, [inaudible 00:15:30] versus a memorial regimen called TICE, which is Taxol, ifosfamide, followed by three courses of carboplatin and etoposide at high dose therapies.
For a variety of reasons, we’ve been champions of phase 3 studies for decades, and we felt that we did not feel comfortable participating in that study because as one of our oncological ethicists talks about, you need to have equipoise when you’re doing a clinical trial, that you can think that either of the two arms can be superior, not just the experimental arm, however you decide which the experimental arm is, can be superior.
So, for the most part, we don’t use standard dose salvage chemotherapy, whether it’s vinblastine, ifosfamide, platinum, or paclitaxel, ifosfamide, platinum, but we tend to use a single course of standard dose chemotherapy, if they’re not platinum refractory and then follow it with two courses of high dose chemotherapy.
We may be wrong in that assessment and may be that the TIGER study will show both arms are exactly the same, but at least borrowing the information from that data, at our institution we are continuing with high dose chemotherapy, rightfully or wrongfully.
Brian:
Larry, talk about the 4-EP versus 3-BEP in good risk terms. Talk about your views on that. I know it’s somewhat controversial.
Larry Einhorn:
Sure. Well, in my opinion, it’s not controversial at all.
Someone asked me a question, why don’t you use EP times 4 for good risk, like Memorial does. And my answer was “because they’re wrong and we’re right.”
Brian:
Of course.
Larry Einhorn:
Memorial, George [inaudible 00:17:11] was one of my best friends and so was Derek Feldman. We’re not even frenemies, we are somewhat competitors in the field. So, we previously did a study in good risk disease where we compare the then standard 4 courses of BEP to the then experimental 3 courses of BEP demonstrating that both arms had a 92% cure rate.
Not even a 1% difference and no difference in progression free survival. And so, we were able to drop that fourth course, which was the most toxic course because of the cumulative ototoxicity, neurotoxicity, anorexia of platinum, and the rare leukemogenic effects of etoposide, which is dose and schedule dependent.
So, three courses and four courses were the same. So, when we look at the two regimens for good risk disease, is BEP times 3 and EP times 4 at Memorial. So, what might logically think the at EP times four might be better because platinum’s a miracle drug. Etoposide is a good drug. Bleomycin is an okay drug, but platinum’s a miracle drug.
Well, we know that 4 BEPs and 3 BEPs were the same. So, there’s no way in the world that 4 EPs is ever going to be superior to 3 BEPs and having treated thousands of patients, the idea of bleomycin with pulmonary fibrosis in young, healthy patients under the age of 50, getting just 3 courses of therapy is a boogieman. We don’t see that.
It’s been 25 plus years since we’ve had anyone who has had clinically significant durable pulmonary toxicity from bleomycin and every randomized study, every single one that has ever been done where the randomization was for or without bleomycin, they have all been numerically superior with bleomycin.
They’re not statistically superior because you would need 1500 patients on a trial because the cure rate is so very high. So, we very strongly feel that if you want to have less neurotoxicity, less ototoxicity less cumulative, anorexia nausea, vomiting, less potential for mild suppressive complications with that fourth course of therapy, it just doesn’t make any sense to us to give 4 courses of EP versus 3 courses of BEP.
You know, I think people have their own ideas about things and I used to be kind of very friendly in conversations about that, but as the years have gone by, I just don’t understand why they use EP times 4 to be honest. I’m sure that Darren would give an equally elegant talk about why [inaudible 00:19:49] doing bleomycin when it could cause Raynaud’s and all these other things.
Tom:
Larry, I got a question on … Brian. You go.
Brian:
No, I was just going to turn away from testis cancer and talk a little bit about sort of elements of career success. Obviously, yours has been a bit of the model and then our since-aborted podcast, you talked a little bit about some of those elements of success early on, early in your career that really led you to where you are today.
Larry Einhorn:
Sure. Was there a question there?
Brian:
Yeah. What, what were the key elements of success for you? What were the … As you look back upon your career, as you say, over 40 to 50 years, what are those key elements?
Larry Einhorn:
So, as I mentioned, when I joined the faculty here, by definition I was treating everything. And you didn’t have to know too much back then to treat everything. I think that today, I only treat lung cancer, Merkel cell tumors, there’s a long story why I do that and testis cancer.
I don’t even do bladder and renal or prostate anymore. I think it’s really hard to be a generalist in this day and age and be knowledgeable in all these diseases. And that’s what makes oncology such an exciting field.
So, I’ve been very fortunate in my career. As I mentioned, I came here to a perfect place where we had John Donohue. As the decades have gone by, the best and the brightest, as you know, are going into oncology rather than someone telling a young resident going into oncology, “why are you choosing this subspecialty when it’s so depressing?”
The science is phenomenal. And we learn from the residents, and we learn from the fellows. And I think when I look back at my career, I view myself as a mentor and a teacher primarily and I love what I do.
And I’m fortunate to be at an academic institution where we have such gifted young people who are so altruistic and are so passionate in their field and this is what I enjoy the most. Yes, it’s a luxury to be treating a curable disease, which makes up about 50% of the patients I see in my clinics with testis cancer.
But it’s exciting also dealing with stage IV B lung cancer with the advances have been made by people around the world with molecular target agents and immunotherapy. And when I was giving this lung cancer lecture, this past weekend, I made the comment that we no longer can say this in hutch terms and tones. We are curing stage 8 B lung cancer. We have people who are out at 10 years on immunotherapy.
We have patients that are out eight plus years on ALK inhibitors with the older drug presentative and they’re continuously disease free, they’re probably cured and who would’ve thought just 10 years ago.
And the other person that was giving the lecture, after my lung cancer lecture, was talking on part T and talking about the incredible advances with [inaudible 00:22:45] and the hemalogical malignancies, and saying that this is the best era to be in oncology. And I was thinking when he said that, in the late 1970s, we thought that was the best era because of platinum, doxorubicin, the nitrosoureas.\
And then as the decades went by and other new drugs became available, we thought that was the best decades. And then 10, 15 years ago, when we looked at eGFR and ALK, and these other molecular targeted agents and of course in renal cell and prostate cancer as well, that’s the best decade. And I think every succeeding decade is going to be the best decade.
I think when we look back at things from previous decades, we’ll probably think that those were a naive way of how we treat cancer. And I think diagnostics have improved tremendously. The knowledge of size has improved logarithmically. And, you look at, in the United States time with the FDA, I was on the FDA oncology advisory committee from 1983 to 1987.
We approve 4 drugs in 4 years. We approve 4 drugs a month now with these newer agents. It’s just a phenomenal field.
Tom:
Larry, do you see yourself predominantly as a researcher or do you see yourself more as a doctor?
Larry Einhorn:
Well, I like to do a little bit of both, and I tend to not be first author in too many publications anymore.
Tom:
Yeah. Brian’s the same.
Larry Einhorn:
Our very brilliant first year, second year, and third year fellows to teach them and mentor them how to put papers or put-up protocols through our IRB. And by the way, talking about that, and I’ve mentioned this before to others, when I wrote the platinum, vinblastine, and bleomycin protocol, from the day I wrote it to the day we treated the first patient was about 4 weeks. Can you imagine that today?
Tom:
Larry, can I ask you a question about Lance Armstrong? He made a controversial contribution to cycling.
Larry Einhorn:
Yes.
Tom:
I’m interested in what contribution he made to testis cancer?
Larry Einhorn:
Well, in the interest of full disclosure, he’s both a friend as well as a former patient. And he has probably done more for the cancer community than any cancer patient has ever done. He raised over a billion dollars, and we banded him about the term survivorship and he and his ex-wife were probably the first people to actually start funding survivorship studies. And yes, he has a checkered career as a cyclist, but everyone did back then.
When he won those 7 consecutive Tours de France, and they took the yellow jerseys away from him, they weren’t giving them to the second, third, fourth, fifth, six place finishers. They were all using performance enhancing drugs at that time. He, back then and today, regularly sends us patients. He’s a hero in the testicular cancer community, although he isn’t a hero anymore, perhaps in all the cycling, yacht community.
He regularly sends patients to us. He, he talks to them on the telephone. He shepherds them to the right research places to go and encourages them.
So, he has done a great deal in that he set up with them was the Lance Armstrong Foundation, which is now the Livestrong Foundation. And they still are very much involved in funding research. So, I think that he may be pillaring by the New York times or Sports Illustrated, but he’s still a hero in the testicular cancer community. And the fact that he raised a billion dollars in a short period of time for cancer research is phenomenal.
Brian:
That I figure’s amazing. I didn’t realize that.
Tom:
Larry, what do you consider your biggest career success and failure?
Larry Einhorn:
Well, it is easy to know what my biggest failure was. Early on, I thought that I could conquer breast cancer. How hard could that be, right? You got hormones, you got chemotherapy, you got all these triggers. And we were early on with the high dose chemotherapy that turned out to be, no pun intended, a bust in breast cancer. And I think that I was not one of the originators, but I was one of the copiers of high dose chemotherapy.
It seemed like an exciting field of breast cancer. It turned out not to be whatsoever, as we know from the [inaudible 00:27:05] phase 3 studies that have been done. And as I would tell my wife, it turned out that breast cancer is a little more complicated than I thought it was. It’s not just a matter of finding the right drug combination and putting it together.
And the other dismal failure is extensive small cell lung cancer. When we treat excessive small cell lung cancer with, albeit a little different dose and schedule of EP of etoposide and platinum, those remissions are just as rapid as they are in testis cancer, but 99% of them relapsed.
And here we are 30 plus years later after the original studies we did with platinum and etoposide and small cell lung cancer, it’s still first line therapy. And the only advance has been a 6 or 7 week advance by adding immunotherapy to the platinum, etoposide doublet. And that’s it, compared to the tremendous advances that have been made to non-small cell lung cancer.
I think my biggest achievement is looking at all the fellows who have done such great work and gone on to academic careers and made such a difference, whether they’re in the United States, outside of the United States, working in the industry, working in the community.
And that’s what I take great pride in. Again, I’ve been very fortunate in my career. I often feel that as an oncologist, we have the best job in medicine. Oncology patients are tremendous. We have a unique relationship with them and among oncologists, I probably have the best job of all of them. I’m dealing with young, healthy, curable patients now as a majority of our patients.
And yes, we have these great advances in lung cancer, but it’s not the same where we can see a new testis cancer patient and tell them that our goal is cure. And we almost always achieve that goal in metastatic testis cancer.
Tom:
Larry, we do a quick-fire round. As you know, we did this last time for you. We’ve devised some different questions. You’ll be pleased to know. Brian, do you want to fire away?
Larry Einhorn:
Oh, you can just ask me the same questions, I’ll give a different answer.
Brian:
The year-end topic of your very first publication?
Larry Einhorn:
Well, because there were no oncologists in the state of Indiana, in all practicality. And I wanted to make myself known to the community in Terre Haute, in Bloomington, in Fort Wayne and South Bend. So, my first publication was probably in the Indiana State Journal, just to let myself be known that there is an oncologist here at Indiana University.
And yes, we need to have patients referred to us. And so that was my first publication and curiously, I kind of replicated that a couple years later in the Connecticut State Journal and I don’t even remember how that came about.
I don’t know whether it was one of my former residents who became an internist in Connecticut and wanted me to do something similar for the Connecticut State Journal. But my first publication was in the Indiana State Journal. You guys probably subscribed to that, don’t you?
Tom:
Yes, we do. And I read it monthly. Francis Crick or Marie Curie?
Larry Einhorn:
I’m sorry. Say that again.
Tom:
Francis Crick or Marie Curie?
Larry Einhorn:
Well, so we’re talking about Madam Curie who won two Nobel prizes.
Tom:
Yeah.
Larry Einhorn:
You got to go with her.
Tom:
Seems reasonable.
Larry Einhorn:
And also, her daughter Irene won a Nobel prize too.
Tom:
What would you-
Larry Einhorn:
I actually tell it to my fellows that if they want to win a Nobel prize it doesn’t matter how hard it works. It’s all genetics. You have to have parents who have won a Nobel prize.
Brian:
What would your career have been if not a doctor?
Larry Einhorn:
Well, I often thought when I was applying to medical school, because I wasn’t exactly what one would call a sterling student in undergraduate school. What I would be doing if I didn’t get into medical school and there was a very real possibility I wouldn’t have gotten into medical school and I probably would’ve gone on as a teacher, hopefully at the university level, not the high school level, teaching biology or chemistry.
Brian:
Love it.
Tom:
Larry.
Larry Einhorn:
I had no athletic prowess and also, I wasn’t going to become a professional athlete.
Tom:
Larry. Rolling Stones or the Beatles?
Larry Einhorn:
Well, the Rolling Stones have been durable. You got to go with them. And at his age he still performs like he was a young stud.
Brian:
What was the favorite location around the world you’ve ever given a talk.
Larry Einhorn:
Australia. I love Australia, despite the 23-hour trip it takes to get there.
Brian:
Yeah.
Larry Einhorn:
It doesn’t matter whether you go East or West, it takes 23 hours. People are great. The scenery is great. It’s just a wonderful place to be.
Tom:
Larry. Memorial or Indiana?
Larry Einhorn:
I’m sorry. Are we giving a memorial to Memorial? Because Indiana is just so far ahead. Actually, in seriousness, I think Memorial Sloan Kettering is the premier cancer institution in the United States, if not the world. And they have just excellence in every field, not just in the GU field, but in testis cancer however …
Brian:
So, Larry. I looked through your CV, I added up the total number of publications, textbook chapters, and abstracts. Tell me what you think that total number is.
Larry Einhorn:
Too many. So that would be 400 plus and 800. Probably about 1100.
Brian:
Yeah, great. I had 1,048 in my math. So pretty close.
Tom:
You’ve obviously done some homework since our last one, Larry, because last time Brian asked that question. You weren’t so sure. I’ve got my last question. George Washington or Abraham Lincoln?
Larry Einhorn:
Well, Abraham Lincoln freed the slaves. George Washington is the father of our country and I think we have to call that one a tie.
Tom:
That’s very politically correct.
Brian:
I think we’ll leave it at that. That’s a good one to end on.
Tom:
Larry. This very fantastic.
Brian:
Thank much for joining us.
Larry Einhorn:
Thank you. It was fun.