The War On Cancer Turns 40

Forty years ago, President Nixon signed the National Cancer Act, beginning the War on Cancer. Harold Varmus, director of the National Cancer Institute, discusses four decades of scientific progress in preventing, detecting and treating cancer—and the mysteries that still remain.

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IRA FLATOW, HOST:

This is SCIENCE FRIDAY from NPR. I'm Ira Flatow. On December 23, 1971, President Richard Nixon sat down to sign the National Cancer Act, beginning what became known as the war on cancer.

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PRESIDENT RICHARD NIXON: More people each year die of cancer in the United States than all the Americans who lost their lives in World War II. This shows us what is at stake. It tells us why I sent a message to the Congress the first of this year, which provided for a national commitment for the conquest of cancer, to attempt to find a cure.

FLATOW: That was Richard Nixon, back in December 23, 1971. How far have we come in the last 40 years? Well, we've learned there's no one, uniform cure for cancer. There's no one kind of cancer, especially as scientists have to come to understand it's not a single disease but hundreds of different ones.

And there's the issue of finding the cancer itself. We've gotten better at that. How do we know when to wait, when to send a patient in for surgery, radiation or chemo? Can we do better at predicting what cancer cells and pre-cancerous cells will do?

What are the promises and the challenges of cancer research? Well, those are questions faced every day by my next guest. Harold Varmus is director of National Cancer Institute in Bethesda. He's also Harold winner of the 1989 Nobel Prize in physiology or medicine for his cancer research, former president of the Memorial Sloan-Kettering Cancer Center here in New York. Welcome back to SCIENCE FRIDAY.

DR. HAROLD VARMUS: Ira, thank you very much.

FLATOW: You reminded me before, you were on 18 years ago the first time.

VARMUS: Indeed.

FLATOW: What has happened in those 18 years? Let me as you first: Let me go back to Richard Nixon's statement. Was it a useful phrase to call it a war on cancer?

VARMUS: Of course, it wasn't Nixon himself who used that term. The term was not in the legislation that he signed. Was it useful? Mixed verdict. I mean, on the one hand, yes, it was good to draw the nation's attention to the fact that this might be a soluble problem.

One of the things that looked strange to me - and I was around doing cancer research in 1971, is the optimism because when - in 1971, we really didn't know very much about cancer. It was essentially a black box. We knew that there were tumors, and we knew that very toxic chemicals could cure some childhood leukemias or at least put them into remission.

And there wasn't the kind of optimism that I feel today among my colleagues and - who feel they have a much deeper understanding of how cancer actually arises and how cancers differ one from the other in different organs, and how even within the same organ we have a much more detailed picture of what a cancer is.

And we've had some successes based on the detailed understanding of how a cancer arises and how a cancer is sustained.

FLATOW: Well, as I said, we know that it's not monolithic, and we've had successes in some, as you say, in some cancers and not in others. Why the difference? Why can we treat some cancers better, some are more difficult?

VARMUS: Well, that's actually an incredibly good question because right now, everyone is quite excited about targeted therapy, that is being able to design drugs or antibodies or other methods that are specifically tailored to either treat the product of a mutant gene or to take advantage of some physiological step like the generation of new blood vessels or manipulation of the immune system in very specific ways to treat cancers.

But we have some cancers that we treat with drugs that we don't understand. For example, since the '70s, we've been able to treat testicular cancer, once a highly lethal cancer, especially young men in their teens and 20s and 30s, with a drug called Cisplatin that we still don't understand.

In fact, one of the things we're trying to do at the Cancer Institute at the moment, despite the fiscal pressure we're under, is to draw people's attention to some really basic things we don't understand, like why does Cisplatin, a drug that doesn't work very well in many common cancers, work so well in the treatment of testicular cancer?

FLATOW: And what other victories have we had in the road in the last 40 years?

VARMUS: Well, I think the one that attracts the greatest attention needs to be mentioned first, is our treatment of chronic myeloid leukemia, a situation - a disease in which we have known for 20 years or more that a specific gene called the abl gene, that makes an enzyme called tyrosene kynase, having a drug that interferes with the action of that mutant kynase can put the disease into remission. And as long as you take one or two pills a day orally, you can maintain that disease in a state of remission so that life expectancy for someone with that leukemia is the same as it would be without the leukemia.

There are other examples of targeted therapies that work well but for a much shorter time because we encounter drug resistance quite quickly in the face of these therapies.

But I think that the thing that we tend to hang our hat on in the realm of treatment - and we want to come back to prevention and diagnosis and other aspects in a moment - but in the realm of treatment, I think the fact that we have the tools now that allow us to analyze the genome, the set of chromosomal information in a cancer cell in so much detail, is giving us a lot of new ideas for treatments, and some of them are very successful, some less so, and others I think show promise that is driving our science in a very, very vigorous way.

FLATOW: Talking with Dr. Harold Varmus this hour on SCIENCE FRIDAY. Our number is 1-800-989-8255. You can also tweet us @scifri, @-S-C-I-F-R-I, leave a message on our Facebook site and our website at sciencefriday.com.

Did we know much about the relationship between viruses and cancers back in those days?

VARMUS: In those days, we knew one incredibly important fact that was very important in my own career, namely that there were viruses in animals that caused cancer, like the rous sarcoma virus of chickens or the meloni sarcoma virus of mice, and those viruses and many others that I won't mention were the tools that allowed us to understand the underlying genetic nature of human cancer.

But now, of course, we know that - and actually began to know in the '70s that there are viruses like the human hepatitis-B virus, the human papillomaviruses, and Epstein-Barr virus and several others, are important in cancer. And we have vaccines against some of these viruses, most importantly the vaccine against human hepatitis-B virus and the vaccine that protects against papillomaviruses that can make a tremendous difference in preventing cancer.

Indeed, the big issue was getting those vaccines into the hands of people who need them, especially in developing countries, and that is a major issue for us. We're taking a big interest right now in cancer in developing countries, some of which have as much as half of their cancers attributable to infectious agents, not just viruses but bacteria like helicobacter that are causative agents of gastric cancer.

FLATOW: Now talking about preventive medicine and taking these vaccines, but I'm thinking back, and I'm - you know, I guess two of the biggest preventable cancers, or we talk about them now, was smoking, right, and there's a huge amount of cancers caused by smoking, and in more recent years melanoma. People talked about not being out in the sun as much or getting sunscreen.

VARMUS: Well, avoiding sun does not completely prevent the appearance of melanomas, but it is one of the risk factors. But your point about tobacco is extremely important. And, you know, we've had some success in this country in reducing the rates of tobacco use to the point where about 20 percent or so of our population smokes. But that's still a very large percentage.

And a very significant - an important point to make here about how we've done in dealing with cancer over the years is that over the last 20 years or so, the age-adjusted mortality rate for cancer has come down about one percent a year.

It's important to use that metric. President Nixon referred to the number of deaths in America. He actually got the numbers a little wrong. There were actually more people killed in World War II, more Americans killed in World War II than dying of cancer each year, but the numbers were not so far off.

But the important - and of course the American population has grown and has gotten older. So you might expect a lot more cancer, and indeed there is - there are more cancer deaths today than there were in Nixon's time. But if you look at the death rate, especially when it's age-adjusted, we've done very well in the last 20 years in bringing down the rates.

Some of that reduction in death rate is due to a reduction in the use of tobacco products. But some is also due to improved surgeries, improved therapies. And numbers like this don't tell the whole story. That's very important to remember, that we've become much more skilled at controlling symptoms of cancer, at demystifying cancer as a disease by trying to explain it scientifically.

The advocacy community has been very good at making cancer something that's not an object of shame so that people live and work - you know, cancer's still a difficult disease. It can be a terrible disease. But we've been much more - we've gotten much better at controlling symptoms and side effects and other aspects of cancer therapy.

FLATOW: And we've gotten so good at actually detecting it at such a very early stage sometimes...

VARMUS: Well...

FLATOW: ...and it's a dilemma.

VARMUS: Yes.

FLATOW: I'm talking - I'm thinking...

VARMUS: Sure.

FLATOW: ...about prostate cancer, you know?

VARMUS: So that - there is a dilemma, and there is a lot of over-diagnoses. We know that cancer arises in a series of steps, and it is possible to see - to find abnormal cells at a time when these cells are not, frankly, cancerous. Cancerous cells invade locally. They metastasize. But some of these early lesions are damages that one can detect, for example, after doing a biopsy in response to a PSA test can lead to an over-diagnosis of cancer and overtreatment. I think that the recent statement by the United States Preventive Task Force about the - their unwillingness to recommend the routine use of PSAs is a very healthy step.

And then, the notion of watchful waiting, if you have a PSA test, as many people do, before the treatment which is often accompanied by really detrimental side effects to the quality of life - incontinence and impotence. These are very healthy developments.

FLATOW: 1-800-989-8255. Let's go to the phones, to Steve in Hotchkiss, Colorado. Hi, Steve.

STEVE: Hi. Thanks for having me on your show. I really appreciate the opportunity.

FLATOW: You're welcome.

STEVE: I'm reading a book called "The China Study," and I was wondering what your guest thought about the effect of nutrition on combating cancer, and I'll take my answer off the air. Thanks.

FLATOW: OK. Thanks for calling.

VARMUS: So the - there's no doubt that what we eat influences cancer rates, and I think probably the strongest evidence for that comes from a lot of historical epidemiological studies in which people are studied when they are in their country of origin and then when they move to other places - Japanese moving to America, Chinese moving to Hawaii and America. And there's no doubt that there are dramatic changes in cancer rates when that happens. One of the things we don't understand is what element of the environment and especially of diet is - can the change in rates be attributed to.

FLATOW: But we - I heard about nitrosamines and things like that in processed meat.

VARMUS: Yes. And that may be one factor that's important, and we have, of course, controlled the use of nitrosamines in meat.

FLATOW: Right.

VARMUS: So I think this is still a very important aspect of what we're - we need to understand about the environmental contributions to cancer rates. And indeed, the NCI has specifically asked that the scientific community to respond to some of these now historically significant observations about changes in cancer rates as people move from one area of the world to another in hopes of getting a clearer picture of what's happening. One of the things that may be helpful is our ability to look at the genomes of cancer cells because we know that the kinds of mutations that you see are reflections of so-called oncogenic cancer-causing agents.

So tobacco smoke or UV radiation from sunlight have signatures that we can see when we examine the genomes of cancer cells, and those may be important in trying to focus our attention on things we eat.

FLATOW: 1-800-989-8255 is our number. We're talking with Harold Varmus, director of the National Cancer Institute on SCIENCE FRIDAY from NPR. I'm Ira Flatow talking with Dr. Varmus. So one thing that has changed since Nixon's time is the obesity epidemic. Is there any connection between obesity and cancer?

VARMUS: There is definitely that connection. It's well-documented that obesity is a risk factor for many types of cancer, not equally across the board. Remember, there are lots of different kinds of cancer. Some of them affect cancer rates by as much as three- or fourfold, some less. It's estimated that if there were no obesity in America, we'd have about 20 percent fewer cancer deaths in this country. And yet we don't really understand what the connection is between obesity and cancer.

One of the things that we're doing with our provocative questions exercise at the NCI is trying to draw people's attention to the fact that this relationship is a highly validated one and ask whether it's a change in inflammatory response or some hormonal effect of obesity that contributes to development of cancer. We are heartened to think that reversing obesity could reverse the high risk of cancer incidence and mortality, and that comes from studies in which people undergo extreme weight loss as a result of so-called bariatric surgery. So while those data are not definitive, they do suggest that you can reverse the risk within a few years, and that's encouraging.

FLATOW: We've always heard - I mean, over the years that I've been covering it there's always been the talk of the magic bullet, you know, the drug that will go right to the cancer and leave the healthy cells alone. And then, there's been talk about tweaking up the body's own immune system. Are we closer to any of those two types of fighting cancer?

VARMUS: Well, no one of us believes in a magic bullet, but we do believe that - well, a magic bullet may not be the best possible metaphor, that there are drugs that will be selective for cancers and selective in two possible ways. One, directing a treatment absolutely at the cancer cells, and there are ways to think about that.

FLATOW: Right.

VARMUS: What's been more widely used are therapies that specifically affect cancer cells because cancer cells have a mutation that makes an abnormal protein that is exquisitely sensitive...

FLATOW: Right.

VARMUS: ...to the drug being used. And we have many examples of that now. The second issue that you raised has to do with the immune system, and for many years, there was a lack of enthusiasm for cancer immunology. That has changed dramatically for two reasons. One is that we have antibodies that are currently used - obviously, a tool of the immune system - that have been shown to work very effectively. We're all familiar with a drug called Herceptin, an antibody that's been around for a long time now that can help control breast cancer and reduce the incidence of metastasis and help to control the growth of metastasis.

But even more exciting, in many ways, is the demonstration just over the last year and the FDA approval of a very different kind of immunological approach, an antibody that confronts or reduces a system - our immune apparatus has for damping down its own activities. So this antibody increases immunological activity by interfering with a naturally occurring suppression mechanism. And that drug, which is now known commercially as ipilimumab is - has been shown to be effective particularly in metastatic melanoma where approximately 20 or 30 percent of patients will have sustained remissions.

FLATOW: Right.

VARMUS: We don't know as yet exactly which patients are most likely to benefit. That's a problem. We'd like to know that. And we don't know as yet which other cancers are most likely to be susceptible to the effects of this modulator of the immune system. But those give us a lot of hope for immune therapies.

FLATOW: After the break, we're going to come back and talk lots more with Dr. Harold Varmus, and later on, a surprising way to turn plastic bottles into bridges, so stay with us. We'll be back with Dr. Varmus after this break. Don't go away.

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FLATOW: I'm Ira Flatow. This is SCIENCE FRIDAY from NPR.

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FLATOW: This is SCIENCE FRIDAY. I'm Ira Flatow. We're talking with Harold Varmus, director of the National Cancer Institute and the winner of the 1989 Nobel Prize in physiology or medicine for his research in cancer. So much to talk about, so little time. Let's talk about how - understanding the human genome. Human genomics is affecting cancer research and cures.

VARMUS: Well, it's affecting it at two levels. One is that it's deepening our understanding of many different kinds of cancer and changing our approaches to making an accurate diagnosis. Moreover, it's becoming part of care, especially at some of our more advanced cancer centers. While patients are being - making decisions about treatment, their genomes are being partially or even entirely sequenced, sometimes illuminating a surprising aspect of their genome that's contributing to their cancer.

And these days, there are a sufficient number of new drugs developed that sometimes possible to pick something off the shelf and make an application of that drug in a way that produces the result when conventional therapies don't work. I foresee a time not very long from now when analyzing a genome in some detail for a $1,000 or $2,000 will give us a very detailed picture of the diagnostic category in which this cancer belongs and a much more sophisticated and precise way of using therapy.

FLATOW: And I know that one part of cancer research and epidemiology that you're especially interested is the differences in outcomes in the U.S. among different kinds of people here.

VARMUS: Yes. It's very important when we talk about how well we're doing or how poorly we're doing and treating different kinds of cancer to take note of the fact that the incidents of cancers do vary among different groups, and the outcomes vary. Among African-Americans in the U.S., for example, for reasons that are not fully understood, some of - may be partially genetics, some - different forms of cancer, different incidents of cancer. Some of it may have to do with the kind of care that people are getting access to.

The death rates and often the incidents are significantly higher. And we need to pay very careful attention to those discrepancies, just as we do when we think about approaching cancer in developing countries where cancer is, I believe, a disease that we need to confront as vigorously as we confront AIDS, tuberculosis and malaria. The incidence varies dramatically among different cancers.

FLATOW: And we don't know why that is.

VARMUS: We don't understand that very well. Sometimes, we can attribute it to viruses that are prevalent in the area, but other times, it's not, and that's an important thing to get hold of.

FLATOW: I want to ask you an interesting question we came up when we talked, you know, we talked about it amongst ourselves. What we have learned and what we can learn from long-lived animals, such as sea turtles, which appear to have very low rates of cancer, right?

VARMUS: Right.

FLATOW: What do they do right?

VARMUS: Well, you're picking up on a provocative question...

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VARMUS: ...and I encourage your listeners to go to the National Cancer Institute website and look at provocative questions. So one of the things that we know that cancer is in general more common as we age, but there are a lot of cancers that occur in childhood or in adolescence or in young adulthood. And then, we look at the size of animals or their longevity, and there's no simple correlation. Mice have a lot of cancers. They're small.

FLATOW: Right, right.

VARMUS: They live for two years. Turtles live a long time, and they're big, and they have very few cancers. Why is that? Maybe we can understand more about the fundamental idiosyncrasies of cancer by paying more attention to these perplexing questions.

FLATOW: Is there something - and I'm sure there is and I'm not sure what the answer of what I'm even asking you - but is there some aspect of cancer, some core aspect that we don't know yet that would help us understand how to combat the hundred or so different kinds of cancer.

VARMUS: Well, one of the things that we're spending - I mean, I think we understand that changes in the genome of a cell whether they're changes that are...

FLATOW: Right.

VARMUS: ...actually attributable to changes in the sequence of bases or rearrangements of chromosomes or changes in the proteins that coat the chromosome and determine gene activity, those are fundamental to making a cancer cell. But the cancer cell lives in an environment where there are blood vessels, immune cells and other - a lot of secreted proteins and hormones and knowing more about the relationship of a cancer to its environment is an aspect of cancer reflected in our new interest in immunotherapy but also in the use of some new therapies, like Avastin, that interfere with the development of an adequate blood supply.

FLATOW: Right, right. There was some thought - it was thought years ago and I guess it was followed up on it if you just starve the cancer cell, take away its blood supply, it's going to go away.

VARMUS: Unfortunately, things don't work out quite as easily as that.

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VARMUS: But there are - this is part of, you know, a multiplicity of approaches to cancer that just as we think about the multiplicity approaches we have to pneumonia...

FLATOW: Right.

VARMUS: ...different organisms treated with different antibiotics, combinations of drugs being very important. We wouldn't be where we are in treatment of AIDS today if we didn't have multiple therapies that allow us to avoid both resistance and attack the HIV virus in a multiplicity of ways. I think that's what will eventually happen with cancer therapies. We'll have several tools for every cancer. Drug resistance will be less frequent and will be more effective as therapies.

FLATOW: Is there any mind-body connection in the literature between, you know, your mind influencing (unintelligible)?

VARMUS: Much speculation. I'm skeptical about most of it.

FLATOW: Yeah, because it's very hard to test for something like that, isn't it?

VARMUS: Indeed.

FLATOW: Yeah. Harold Varmus, thank you very much, as always, for taking time to be with us.

VARMUS: My pleasure, Ira. Thank you very much.

FLATOW: A consistent returning guest to SCIENCE FRIDAY, Harold Varmus is director of the National Cancer Institute in Bethesda, also the winner of the 1989 Nobel Prize in physiology or medicine for his cancer research. He was joining us in our New York studios. Have a happy holiday season to you.

VARMUS: Thank you. You too, Ira.

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