Skip to main content

The 5 Best Dramas on T.V. Right Now.

TV critic David BIianculli gives us his top-five favorite TV dramas. "Homicide: Life on the Streets," "NYPD Blue," "Ally McBeal," "The Practice," and "Buffy The Vampire Slayer"

05:53

Other segments from the episode on February 16, 1999

Fresh Air with Terry Gross, February 16, 1999: Interview with Robert Weinberg; Commentary on television dramas.

Transcript

Show: FRESH AIR
Date: FEBRUARY 16, 1999
Time: 12:00
Tran: 021601np.217
Type: FEATURE
Head: Robert Weinberg
Sect: News; Domestic
Time: 12:06

TERRY GROSS, HOST: This is FRESH AIR. I'm Terry Gross.

Cancer is one of American's greatest health fears. Cancer may be a reality for you or someone close to you. This week we're presenting a series about cancer focusing on the latest research and how people with cancer can best arm themselves with useful information.

We begin the series by asking, what is cancer? How do cancer cells form? And how do they develop into tumors? My guest, Dr. Robert Weinberg is the author of the new book "One Renegade Cell: How Cancer Begins." He is a researcher who is a pioneer in the genetics of cancer cells.

In 1997 he was awarded the National Medal of Science. Weinberg is the Director of the Oncology Research Lab at MIT's Whitehead Institute, and Professor of Biology at MIT. He says that cancer is a disease of faulty information processing deep inside cells.

I asked him to explain.

DR. ROBERT WEINBERG, AUTHOR, "ONE RENEGADE CELL;" DIRECTOR, ONCOLOGY RESEARCH LABORATORY, WHITEHEAD INSTITUTE: Well, 20-30 years ago we still had no idea how cancer really began. We knew that there were tumors. We know tumors had billions -- tens of billions -- of cells in them. But we never knew why the cells within the tumors were misbehaving.

And over the last 20 years, cancer researchers have picked apart the cells. Looked into the innards of the cell. Look at the machinery which makes normal cells grow and enables cancer cells to grow in an uncontrolled fashion.

And what's come out of the studies of this research -- very basic research -- is the realization that a cell works sort of like a computer. That it processes a lot of information, much of it coming from its surroundings. And on the basis of different signals that it receives the cell decides whether or not it should grow.

In the case of a cancer cell we have a situation where the minicomputer inside the cell is misprocessing information and telling the cell to grow, when by all rights the cell should be stopping growth and really being quiet.

GROSS: What's causing this little computer inside the cell to give it such damaging information?

WEINBERG: Well, then we step one step back and ask, "how does this computer get assembled? What put's it together?" The fact of the matter is the individual components of the computer are templated by genes. So every cell has a set of genes in it, and these genes specify the different interconnecting components of the computer. And together they figure out the logic of whether the cell should grow or not.

And when cancer arises we have a situation where these blue printing genes that normally determine the configuration of the computer and the wiring diagram of the computer, these blue printing genes become damaged and in turn the components of this minicomputer then begin to malfunction.

GROSS: Are these damaged genes part of your genetic makeup when you're born, or do they get damaged as your life goes on?

WEINBERG: The great majority of these genes are damaged during the course of your lifetime as a consequence of diet or smoking or lifestyle. Some of us, however, are unfortunate enough to be born with damaged genes.

And if one is born with damaged genes then one has a much greater than normal risk of coming down with cancer. But in general, probably between 90 and 95 percent of cancers in the American population are due to genetic damage that occurs post-natally, after one is born into this world.

GROSS: You say that unlike regular cells, cancer cells disregard the needs of the community of cells around them. They're only interested in their own proliferation. They are selfish and unsociable. What does that mean?

WEINBERG: Well, you have to realize that the human body is made of something more than 10 to the 13th cells. That's something like 10,000 billion cells in one large body. And in order for these cells to coexist in an orderly way, they have to be talking with each other at all times. They have to be informing each other of one another's needs. And one or another cell in the body can't all of a sudden decide to launch forth on its on and start proliferating -- start multiplying.

Consequently, there's constant intercommunication going on as if different people living in an apartment house were constantly talking with one another -- incessantly talking with one another. And when a cancer starts one of these cells begins to ignore the information -- the signals -- that it's getting from all the other cells in the tissue and begins to multiply, oblivious to whether the other cells want it to multiply or not.

GROSS: And is it the mutated gene that gives it the signal to just go it's own way and keep proliferating?

WEINBERG: Exactly that. The mutated gene, either enables the cell to ignore the information it's getting from its neighbors or, as is often the case, the mutated gene actually pushes the cell to grow incessantly independent of any outside signals the cell may be getting.

GROSS: And as the cell keeps multiplying it eventually becomes a tumor.

WEINBERG: Exactly. It's a little more complicated than that because the development of a human tumor often takes 20, 30, 40 even 50 years. And as a consequence as we grow older each of us might have small incipient tumors forming in various parts of the body, but we don't live long enough for them to bear fruit in terms of actually becoming apparent. Most of them don't have enough time to develop properly.

And in addition you have to say that when a normal cell becomes converted into a cancer cell it's not just one gene that becomes mutated, there's a whole series of genes that must become mutated in succession. It's not just one short circuit that must occur in the wiring of the minicomputer, there must be several of these short circuits occurring in order for the cell really to begin running amok.

GROSS: My guest is cancer researcher Robert Weinberg whose new book is called, "One Renegade Cell." He's also a professor at MIT.

Now you said that carcinogens can wreak havoc on the genetics of cells, thereby creating cancerous cells. Can viruses do that too?

WEINBERG: Viruses can also wreak havoc on cells. If you ask, in the American population, how often do viruses actually succeed in creating cancer; it's actually relatively little. Certainly cervical carcinoma, which is declining rapidly, is created by a viral infection -- human papaloma (ph) virus.

And certainly AIDS patients, because of their immuneo (ph) compromised state, succumb often to copley sarcoma (ph), which is also caused by a virus. And on occasion people who have chronic lifelong Hepatitis B virus infection, they come down with liver cancers.

But the great majority of cancers in our country are not due to an infectious agent such as a virus. They are due to genetic damage, mostly due to chemicals which enter the body and damage genes in one cell or another.

GROSS: We've talked a little bit about how genes of a cell can get mutated and create cancerous cells. There is also something called tumor suppressor genes. What are they?

WEINBERG: In fact, the way that the wiring is rigged up inside ourselves is that there are some genes, and therefore some components of these minicomputers, which push the cell to grow. And there are other genes which hold the cell back.

And these two kinds of genes and proteins are constantly fighting with each other. Some forcing the cell to grow, others holding it back. And often when one creates a cancer cell, what is seen is that the growth promoting genes become hyperactived almost like a stuck accelerator in a car.

And conversely, the growth inhibiting genes, sometimes called tumor suppressor genes become inactivated. So that the breaking mechanism of cells therefore becomes defective. And consequently some people liken a cancer cell to a runaway car where the accelerator pedal is stuck to the floor, and the braking system -- the brake lines -- are defective.

GROSS: So if scientists could figure out a way how to fix the brakes, so to speak, would that be a clue to stopping cancer?

WEINBERG: That would be a way to stopping cancer. In principle, one might want to reinsert into cancer cells the genes which once again reactivate the braking mechanism. The problem is that such a strategy, which is often called "gene therapy," is very hard to carry out.

It's very hard to insert genes back into cancer cells with any efficiency. And if you therefore have a billion or 10 billion cells forming a tumor mass, it's hard to ensure that you can deliver such a braking gene back into all of them. Thereby shutting down the growth of all the cells in that tumor cell population.

GROSS: Now there's another mechanism within cells which is a kind of suicide mechanism. This is within cancer cells. Would you explain what that is?

WEINBERG: It turns out that all the cells in our body are wired to commit suicide rather quickly if something goes awry. And therefore, we're constantly eliminating cells which are defective in one or another way by flipping a switch -- that is the cells are flipping a switch inside them -- which triggers this suicide program, which enables a cell to kill itself within an hours time which is pretty quick.

And this suicide mechanism is sometimes called "apoptosis" (ph). We now realize that this hard wiring in the minicomputers inside cells is set up so that if cells start growing inappropriately -- incipient cancer cells start growing inappropriately -- this apoptotic suicide mechanism will trigger thereby eliminating the cell.

And therefore we conclude that often when you actually see a cancer cell growing it's a cell which has somehow evaded this suicide mechanism and learned to survive in spite of the fact that this suicide mechanism has been threatening it's very survival. It's evaded the suicide mechanism.

Often when we treat cells with chemotherapy what we're actually doing is not bludgeoning the cancer cell over the head with some toxic chemical, really these chemo therapeutic compounds, to the extent they work, succeed by triggering the switch inside the cancer cell which in turn is able to activate the suicide program.

GROSS: Are scientists learning more how to activate the suicide program through chemotherapy drugs?

WEINBERG: Over the last three or four years our understanding of this suicide program -- this apoptotic mechanism -- has increased enormously, by ten-twentyfold. And in fact the development of new kinds of chemo therapeutic drugs is focused increasingly on figuring out ways of doing just what you say: turning on the suicide program inside cancer cells causing them to kill themselves while at the same time sparing the lives of nearby normal cells.

GROSS: Are these new therapies less toxic to healthy cells?

WEINBERG: That's the hope, but the reality is still a bit elusive.

GROSS: Right. Because the therapies for cancer are sometimes so horrible to endure.

WEINBERG: They're unacceptable because of all of these toxic side effects. And therefore with this understanding of how the suicide machinery is wired up inside cancer cells and inside normal cells one hopes now over the next five years to be able to deliver drugs, or develop drugs at the very least, which will be very selective for killing cancer cells while sparing normal tissue. Thereby minimizing the side effects of chemotherapy.

GROSS: My guest is Robert Weinberg. He's a cancer researcher who directs the Oncology Research Lab at the Whitehead Institute. He is a professor at MIT. Winner of the 1997 National Medal of Science. And author of the new book, "One Renegade Cell." Let's take a short break here and then we'll talk some more about cancer.

This is FRESH AIR.

BREAK

GROSS: My guest is Dr. Robert Weinberg. He's a cancer researcher and author of the new book, "One Renegade Cell: How Cancer Begins."

Let's look at the difference between tumors and regular tissue. You describe tumors as taking on the appearance of alien life forms. Can you describe a little bit from a scientists point of view how a tumor looks different from regular tissue?

WEINBERG: Well, if you look at regular tissue under the microscope you see that there are layers of cells that are very well organized. And they array themselves in specific shapes so that they can do certain functions. Cells in the gut are responsible for absorbing food. Cells lining the cavities in the lung are responsible for absorbing air.

All of these different functions require very detailed architectural design at the microscopic level. But if you look at a tumor then you see a big jumble of cells that has no architectural integrity. These are just cells growing willy nilly, every cell out for itself. These are cells which are not intent at all on creating any higher structure.

All they are interested in, if you want to be a little anthropomorphic, all these cells are interested in is making more copies of themselves.

GROSS: Now you say that tumor cells require constant nourishment and oxygen. And they also have to continuously rid themselves of carbon dioxide and other waste products of their metabolism. So what do they do different from regular cells in terms of nourishing themselves and excreting their wastes?

WEINBERG: When a cancer starts inside the body, that is a cluster of cancer cells, it has a serious problem. Because when the tumor cell mass reaches a size of about a millimeter, which is maybe, let's say, an eighth of an inch, something like that; then all of a sudden the thousand or so cells -- or the million or so cells in that small mass can no longer proliferate because it starts running out of food. It starts running out of nutrients and oxygen, and it can't get rid of all the metabolic wastes and carbon dioxide.

So this little clump of cells might just sit there for years half starving because it can't expand anymore. In fact, this is quite intentional on the body's part. The body makes this mechanism work so that many small clumps of incipient tumor cells aren't able to progress any further.

And indeed, as I mentioned earlier, our bodies are probably riddled with little masses of pre-malignant cells that are unable to expand above anything more than an almost microscopic size. So the question is then, how do these small masses of tumor cells solve the problem of acquiring nutrition and getting rid of metabolic waste?

And what they do, if they are going to be truly successful in forming a malignant tumor, is the following: they send out a signal, or they learn how to send out a signal, to normal tissue nearby telling the blood vessels in the normal tissue nearby to start growing from the normal tissue into the tumor mass.

And when this happens, now these blood vessels begin to carry in nutrients into the tumor mass and carry out carbon dioxide and chemical wastes. This is a process that is sometimes called "angiogenesis." (ph) It's only recently been discovered and elucidated in great detail by a surgeon in Boston named Judith Faulkman (ph). And it represents an aspect of tumor formation whose importance was only appreciated recently.

GROSS: So basically is the tumor hijacking your blood system?

WEINBERG: The tumor cells are parasitizing the normal blood vessels. They are acting as parasites. But they have to learn how to seduce the normal blood vessels to grow into the tumor mass. And the way they do that is they send out certain chemical signals which then persuade the normal blood vessels to begin to penetrate into the tumor mass thereby bringing in these much needed nutrients.

GROSS: And can the tumor also use these new blood vessels growing through the tumor to send renegade cells out to metastasized the cancer?

WEINBERG: That's a very interesting question, because a final step in the progression -- in the development -- of a tumor is that certain cells within the tumor mass learn to become pioneers and settle elsewhere in the body -- the process of metastasis.

And that raises the question how they get from one part of the body to the other. How do they get from the primary tumor to the site where they eventually land? Often they will migrate through blood vessels. Other times they'll migrate through lymphatic vessels that go through the body's tissues as well.

And clearly, as you implied, if there are blood vessels that are coursing through a tumor mass they might represent a very attractive avenue for tumor cells to break off from the primary tumor mass, float through the circulation and settle down somewhere else in the body. Thereby founding a new colony of tumor cells.

GROSS: Now cancer cells seemed to really want to reproduce, I mean, the way you describe it its like their goal in life is to just reproduce and keep spreading. And metastasis, I guess, is kind of part -- part of the plan there. But is it hard for the cells -- the cancerous cells -- to survive in other parts of the body once they've traveled through the circulatory system or the lymph system to another organ?

WEINBERG: One imagines that there are, with great frequency, pioneer cells that break away from a primary tumor and try to settle elsewhere. And only one in a million occasions or one in ten or a hundred million occasions do they succeeded in actually founding a colony -- a metastasis -- somewhere else.

Because there are a lot of obstacles in their path. Tumor cells don't survive well in the blood. They don't stick well to foreign sites. Once they do land in a foreign site often the environment is quite hostile for them. So it's only on rare occasions that a metastasizing cell will actually succeed in forming a new colony. Which may be the reason why metastasis is not even more frequent than it is in human cancers.

GROSS: Why do tumors often spread to predictable places? For example, people with lung cancer often develop tumors in the brain or the liver. People with breast cancer often develop bone cancer.

WEINBERG: The short answer to that is we don't really know. The speculation is that the sites to which they home are particularly hospitable and encouraging for their growth. So that breast cancer cells might, for example, find an especially hospitable home, for reasons we don't understand, within bones for example. But beyond that, the precise biochemical explanation of why they find it hospitable are still elusive.

GROSS: It's possible for people to live with cancer for a fairly long time before they even have any clue that something is wrong. I mean, sometimes by the time a cancer is diagnosed it's pretty advanced. And it's kind of amazing that someone has been able to live with it with so few symptoms.

And then often once it gets advanced the symptoms just keep coming and it's hard to carry on. How is it possible to have a large tumor that's metastasized and still not feel much in the way of symptoms?

WEINBERG: A large tumor mass could be growing, for example, in your abdomen. And as long as it's not pressing in any serious way on one of the organs in your abdomen you might never know it's there. Tumor cells are pretty much like normal cells.

So the very fact that they are present doesn't necessarily give any indication that there may be a large tumor mass around. Usually one only begins to sense the presence of a tumor when its size becomes so large that it begins to compromise the function of the kidneys or the liver or the lungs or the heart. Only then does one begin to realize that something is amiss.

GROSS: What does the cancer do that so compromises the person who has cancer that the cancer kills them? Is it usually because of an obstruction or because of a total -- a problem with the circulatory system with blood counts going bad because of the cancer or all of those things?

WEINBERG: Sometimes a tumor can obstruct the operations of the colon and therefore one can't digest. Often colon tumor cells will invade into the liver. And then the liver cells can no longer do their normal function because they're being crowded out by the cancer cells that have started to grow in their midst.

Sometimes the cancers will invade into the pancreas or into the brain or into the kidneys. And in each case the functioning of the organ will be compromised by an ever increasing mass of proliferating cancer cells.

GROSS: Dr. Robert Weinberg is the author of "One Renegade Cell: How Cancer Begins." He's the director of the Oncology Research Lab at MIT's Whitehead Institute. he'll be back in the second half of the show.

I'm Terry Gross, and this is FRESH AIR.

BREAK

GROSS: This is FRESH AIR. I'm Terry Gross.

Back with Dr. Robert Weinberg. He's a cancer researcher who was awarded the National Medal of Science in 1997. He directs the Oncology Research Lab at MIT's Whitehead Institute. His new book is called "One Renegade Cell: How Cancer Begins."

You've done a lot of cancer research over the years, and one of your areas of specialization is the genetics of cancer. Could you describe for us what your findings have been in that area?

WEINBERG: Well, when we talk about cancer genetics we're really talking about two kinds of genetics: one, the genes that you're born into the world with. Are they good genes or are they defective genes. And the other kind of genetics is the genetics of the genes that suffered damage during your lifetime. Those kinds of genetics, the genes that suffer damage during your lifetime, are responsible for the vast majority of cancers in our population.

In both cases what's of central interest is how the damage to specific genes inside a cell actually causes that cell to misbehave. Inside a human cell are probably upwards of 80,000 genes. And only a small number of those genes -- between five and ten -- must suffer damage before the cell begins to grow in a malignant fashion.

And so the goal of many people in my field of research has been to find those few genes; figure out how they suffer damage; figure out once they suffer damage why the cancer cell grows abnormally. And then figure out how to exploit that information to develop new kinds of diagnosis and, ultimately, therapies.

GROSS: What do you think the impact of the human genome project, which is mapping the genes of the human body, is going to have on cancer therapy?

WEINBERG: The impact on cancer therapy, initially at least, will be quite indirect. One of the problems in my field of research has been to find the genes which suffer damage inside cancer cells and understand why they cause cancer cells to grow abnormally.

And the search for these damaged genes has been very difficult -- very arduous. Each one represents a major triumphant, finding the small needle in a very large hay stack. I mentioned that one of these genes may only be one out of 80,000 genes inside a cancer cell.

Once the sequencing of a human genome progresses and succeeds, the search for these cancer related genes -- these cancer causing genes -- is going to be enormously accelerated. And so what might have taken us, in the past, five years to find might then happen in five weeks.

And consequently, a decade from now we'll have a much more complete listing of the repertoire of genes which, when damaged, lead to the formation of cancer cells. And that, in turn, will facilitate the development of therapeutics because the new generation of anti-cancer therapeutics is going to be targeted to the products made by these genes.

In other words, for the first time we'll be able to figure out rationally how to craft -- how to create -- new kinds of anti-tumor therapeutics based on the information of why and how the cancer cells are growing abnormally. Until now it's all been hit or miss, we've not really been able to develop chemo therapeutics on the basis of any knowledge of why cancer cells are growing abnormally.

GROSS: Tell us a little bit about the therapies that might be on the horizon that will connect to the information about the genetics of cancer cells. In other words, as scientists like yourself find out more about cancer genes how might new therapies tie-in with that?

WEINBERG: By studying some of the genes that control the suicide program inside cancer cells we begin to understand how the wiring diagram of that little minicomputer operates. And a number of new developments in the anti-cancer field are going to come from hitting certain of the proteins inside cells that are responsible for preventing cancer cells from committing suicide.

If you inactivate an anti-suicide protein that will in turn trigger the cancer cell to kill itself. And so the genes that control the suicide program will lead directly to new ways of killing the cancer cell.

Another exciting avenue of approach is to try to figure out how to prevent blood vessels from invading into the tumor providing it nutrition. I mentioned earlier that this in growth of blood vessels is called angiogenesis. And therefore there is research, which is currently ongoing and very active, trying to craft new kinds of chemical compounds that prevents the in growth of these blood vessels, thereby depriving the tumors of vital nutrition.

Once again, that's a very exciting area. So far its not yielded very much in direct clinical benefit, but I'm very optimistic that over the next five years it will.

GROSS: Now what specifically are you looking at now in your genetic research?

WEINBERG: Part of my laboratory is focused on yet another aspect of cancer cells that we haven't talked about today, which seems to be equally vital for their ability to proliferate and ultimately to kill the cancer patient. And this other area of work derives from the observation that cancer cells seem to be immortal.

And when I talk about immortal I don't mean that an individual cancer cell is immortal, what I mean is that if you put an individual cancer cell into a Petri dish it can multiply forever -- once a day, indefinitely. In contrast, if you put a normal cell from a normal tissue into a Petri dish and tried to propagate it it will grow for a certain fixed number of doublings -- 40, 50, 60. And then it will stop growing.

Somehow it's run out of its allotment of generations. And this has been a great puzzle in the field of cancer cell biology for many years. Until some years ago certain scientists proposed a mechanism by which normal cells stop their proliferation, and by which cancer cells acquire the ability to break through this mortality barrier acquiring the ability to grow forever.

In fact, one has learned that much of this immortality of the cancer cell derives from a certain enzyme called telomerase. And the telomerase enzyme, when it's inappropriately active inside cancer cells, enables them to proliferate virtually forever. Whereas that enzyme is not operating, one believes, in most kinds of normal cells.

So this aspect of unlimited growth is critical to cancer cells. In the absence of being able to grow in an unlimited fashion a tumor could never grow to a size where it would be life threatening.

GROSS: So what clues into new therapies does the existence of telomerase give you?

WEINBERG: Well, telomerase, amusingly enough, is very similar to an enzyme that HIV virus uses to replicate when it infects cells. It's called a reverse transcriptase (ph). And the fact of the matter is that very successful anti-HIV therapies have been made by developing chemicals that prevent the enzyme of HIV from operating. Thereby compromising the ability of HIV to replicate and kill the patient.

And one has every reason to think that over the next several years -- three to five years, not 50 years but three to five years -- one will develop new kinds of chemicals that interfere with the operations of this telomerase. Quite similar in its overall structure to the HIV enzyme.

And once one interferes with the telomerase one may be able to cause cancer cells to actually revert to normal growth or to kill themselves. Indeed, preliminary experiments already online suggest that that's a very attractive strategy for developing new kinds of anti-cancer compounds.

GROSS: My guest is cancer researcher Dr. Robert Weinberg. We'll talk more after a break.

This is FRESH AIR.

BREAK

GROSS: My guest is cancer researcher Robert Weinberg, author of the new book "One Renegade Cell."

What's the most exciting research your lab is involved with now?

WEINBERG: Well, my laboratory is focusing on this telomerase enzyme which enables cancer cells to grow without limits. I'm very excited by that because it offers a very attractive target for developing new kinds of anti-cancer compounds.

And we're also trying to understand how breast cancer starts, because interestingly enough one really doesn't understand how most human breast cancers begin. One doesn't really understand what genes suffer damage in these cells that causes them to grow abnormally.

And so we're studying the inception of breast cancer by studying breast development in mice and how one can alter a perturbed development of the normal breast tissue in the mouse. That promises to yield many insights into how human breast tissue develops normally and how it misdevelops during the formation of breast carcinomas -- of breast cancers.

GROSS: Now is breast cancer very different from other forms of cancer in terms of what sets it off?

WEINBERG: Each tumor in a different part of the body has a different set of factors that set it off. In the case of human breast cancer, for example, there are a lot of hormonal factors that are very important. For example, the number of menstrual cycles through which a woman goes through in a lifetime may be an important causative factor for breast cancer, but it's totally irrelevant to her susceptibility to colon cancer.

And consequently one has to look at hormones and how they influence the proliferation -- the multiplication -- of cells in the normal breast and try to translate that information into understanding how breast cancers begin.

GROSS: Now how does the number of menstrual cycles a woman goes through affect how prone she is to cancer -- to breast cancer?

WEINBERG: Because each time a woman goes through a cycle there is a whole burst of hormones -- of steroids -- which induces, temporarily, the proliferation of cells in her breasts in anticipation that she may become pregnant.

And each time there is this proliferative stimulus, each time these cells are goaded into growing there is a risk that something may go awry. And consequently the more times that there are the stimuli coming from hormones the greater proportionately, one believes, is the risk for breast cancer eventually appearing.

GROSS: And that has led you or you and other scientists -- I'm not sure if this is your theory or not -- that one of the reasons why there might be a rise in breast cancer is that women are menstruating earlier, at a younger age, than they used to. And also many women either aren't having children or having fewer children than their predecessors, and consequently they're going through more menstrual cycles because they don't menstruate when they're pregnant.

WEINBERG: Exactly. There's a fascinating statistic which says that a modern American girl in 1999 may go through more menstrual cycles by the time she's 18 than her great-great-grandmother would have gone through in an entire lifetime. Simply because she began cycling earlier, she has no pregnancies and lactations which impede cycling, and she will continue to menopause much later in life.

But already by the age of 18 she will have gone through many more cycles than her ancestors of 150 years ago.

GROSS: But not all breast tumors are receptive to estrogen or are sparked to grow by estrogen are they?

WEINBERG: You're absolutely right. There is really two major classes of breast cancers: those that are driven to grow by estrogen and others that are driven to grow by another more complex set of growth factors. And we don't really understand the origins of these two classes -- these two major classes of breast cancer. They represent a puzzle, but a puzzle that I believe will be solved within the next decade.

GROSS: If you're just joining us my guest is Robert Weinberg. He is a cancer researcher and author of the new book, "One Renegade Cell: How Cancer Begins."

When you started doing cancer research as a young scientist in the early '70s did you know anybody who had cancer? Was cancer a reality in your life?

WEINBERG: It was. My mother died of cancer in 1971 -- quite a few years ago. So it was a reality in my life.

GROSS: That's while you were researching already, right?

WEINBERG: It was in the midst of my studies, but it wasn't really the reason why I went into cancer research. The reason I went into it then and continue to have done it is it's been very interesting and very challenging. And I go to the lab everyday really because I look forward to helping to solve certain interesting problems with the hope that some of these problems, once solved, will eventually lead to helping people out.

But one has to understand that the kind of work I do is often 10 or 20 years removed from actual application in the cancer clinic.

GROSS: I think, you know, when you're around cancer you almost start to think that it's impossible not to get it. I mean, there is so much cancer now. At least it seems that way.

WEINBERG: Can I come back on that one?

GROSS: Yeah. And I'd also like to know since you're thinking about cancer all the time if it's made you any more fearful of getting it or anymore -- yeah, fearful of getting it?

WEINBERG: Well, of course it is said that the greatest hypochondriacs are medical students who begin to learn all the things that can go wrong with the human body. But let me talk a little bit about epidemiology.

The fact of the matter is if you don't smoke the risk of getting cancer now is actually a little bit less than it was 60 or 70 years ago. So it's not as if we're being inundated by an epidemic of cancer. To the extent that there are many more cases of cancer in this country than there used to be, it's really two factors: first of all, most of the increased rate of cancer comes -- virtually all of it -- comes from tobacco.

If you subtract the effects of tobacco away, then the rates of most kind of cancers would be pretty flat. In fact, the mortality from breast cancer now is exactly what it was 60 years ago. The other factor is that the human population is growing older, especially in this country. And cancer is largely a disease of old people.

Colon cancer, for example, is a thousand times more likely in a 70-year-old man than it is in a 10-year-old boy. And therefore as the population ages the number of cases of cancer increases. But again, I'll repeat, the risks of a 70-year-old woman coming down with cancer in 1999 are, in the absence of tobacco use, virtually identical to the risk of a 70-year-old woman coming down with cancer in 1930.

GROSS: I'd like you to leave us with one of your hopes for the future. With a new therapy that you hope will tie-in with a new understanding of how cancerous cells reproduce. Something that you think is within reach and that you might see in your lifetime.

WEINBERG: I think within my lifetime -- I don't want to presume, since everyday is a gift -- I think within my lifetime we can very reasonably expect, indeed over the next decade, potent anti-telomerase inhibitors that cut short the growth of immortalized cancer cells.

Potent anti-angiogenic factors that prevent the in growth of blood vessels into tumors. And pro-aproptotic compounds -- compounds that trigger the suicide program of cancer cells. Each of these are very realistic and very plausible within the next decade.

GROSS: Any final thoughts about cancer and its treatment for us?

WEINBERG: Many people think that the greatest improvements in cancer treatment and the greatest reductions in cancer mortality will come from the development of new generations of treatments -- new kinds of anti-cancer compounds. But the reality is that the greatest reduction in cancer deaths will come from prevention. Far greater than anything that doctors can do confronting an already developed cancer.

We could cut the cancer rate by a factor of two -- the cancer death rate -- by a factor of two tomorrow if people stopped smoking and began to change their diets away from high fat, high meat diets to a largely vegetarian diet. It would have a dramatic effect on decreasing cancer death rates. Far more dramatic than anything that people like myself could do.

GROSS: Well, I wish you really good luck with your research. And I'm glad you're doing it. Thank you very much for talking with us about cancer.

WEINBERG: Terry, thank you very much for having me.

GROSS: Dr. Robert Weinberg is the author of "One Renegade Cell." He's Director of the Oncology Research Lab at MIT's Whitehead Institute.

Last week, shortly after our interview was recorded, scientists at the National Cancer Institute announced they had successfully duplicated the promising results of experiments using drugs to cut off the blood supply to cancerous tumors in mice.

The Institute is preparing to test two related drugs, Andostaten (ph) and Angiostaten (ph) on humans. The first phase of the testing is to determine whether the drug is safe for people. If the drug passes this phase their effectiveness will be tested.

This is FRESH AIR.

This is a rush transcript. This copy may not
be in its final form and may be updated.

TO PURCHASE AN AUDIOTAPE OF THIS PIECE, PLEASE CALL 888-NPR-NEWS

Dateline: Terry Gross, Washington, DC
Guest: Robert Weinberg
High: Robert Weinberg is the author of the new book "One Renegade Cell: How Cancer Begins." Weinberg talks about how cancer develops and what can be done to stop it. He is director of the Oncology Research Laboratory at the Whitehead Institute in Massachusetts. He is also a professor of Biology at the Massachusetts Institute of Technology in Cambridge, Massachusetts. He is also author of "Racing to the Beginning of the Road: The Search for the Origin of Cancer."
Spec: Cancer; Diseases; Lifestyle; Culture; Robert Weinberg

Please note, this is not the final feed of record
Copy: Content and programming copyright 1999 WHYY, Inc. All rights reserved. Transcribed by FDCH, Inc. under license from WHYY, Inc. Formatting copyright 1999 FDCH, Inc. All rights reserved. No quotes from the materials contained herein may be used in any media without attribution to WHYY, Inc. This transcript may not be reproduced in whole or in part without prior written permission.
End-Story: Robert Weinberg

Show: FRESH AIR
Date: FEBRUARY 16, 1999
Time: 12:00
Tran: 021602NP.217
Type: FEATURE
Head: David Bianculli
Sect: Entertainment
Time: 12:50

TERRY GROSS, HOST: Our TV critic David Bianculli says it's been up and down year for TV's dramatic series. And when looking at the five best dramas on primetime TV right now he says there are a few surprises and one potential shock
.
DAVID BIANCULLI, TV CRITIC: If you'd asked me two years ago, or three or four, to name the best drama series on TV my answer would come immediately and emphatically: NBC's "Homicide: Life on the Street." But for several reasons that's not true anymore.

For one reason, "Homicide" got softer this season, at least in the first half, and lost its focus and some of its edge. Since January, the stories have gotten stronger again, although one recent episode about a murderer who broadcast his killings live on the Internet felt more like a leftover script from "Profiler" than a "Homicide" original.

Another reason "Homicide" has slipped from the top slot, in my personal ranking of TV's best primetime dramas, is that "NYPD Blue" has gotten so much better this year. The way the show said goodbye to Jimmy Smits' Bobby Simone and has made room for Rick Schroeder's Danny Sorensen really gave "NYPD Blue" a boost.

The nice touches and twists keep coming too. In tonight's episode one more familiar character dies and another one joins the squad room as a weekly regular. So right now at this point in the season, I'd have to rank "NYPD Blue" above "Homicide."

And above them both in the top slot I'd put "The Practice." The David E. Kelley courtroom drama that this year has the best scripts and a lot of the best acting on network TV. You can also find great scripts and great acting on "Ally McBeal," Kelley's other TV show. But that show classifies itself as a comedy.

Actually, it's one of those ambitious hybrids that television has never found a good name or category for. Back when "Lou Grant" spun off Ed Asner's character from the "Mary Tyler Moore Show" into an hour long series -- 21 years ago -- it was called a drama even though plenty of scenes were played for laughs.

On the other hand, even though "M*A*S*H" got very serious at times it always was considered and classified a comedy. Other groundbreaking semi- serious half hour comedies like "The Days and Nights of Molly Dodd" and "Frank's Place" were called "dramadies." A terrible stupid word that never really stuck.

By the time "Northern Exposure" mixed comedy and drama in a one hour format it was called a drama period, and even won an Emmy for Best Dramatic Series. Even though its creators, in their acceptance speech, admitted they really considered it a comedy.

The truth is any show that has got enough drama in it to make you cry and enough comedy to make you laugh should be eligible in either category. That's why I'm adding "Ally McBeal" to my list of TV's top five dramas. And it's also why I'm adding what I consider to be the shocker on this list, the WB series "Buffy the Vampire Slayer." You heard me correctly.

Yes, this series is about high schoolers who band together at night to save their community and the world from vampires and zombies and other demons that just happen to be drawn to the neighborhood hellmouth. And plenty of the scenes and lines are laugh out loud funny, but "Buffy" also has more romantic angst than just about any other TV show on the air these days. As well as real characters who react in real ways to their often very unreal experiences.

Last week, for example, Sarah Michelle Gellar's Buffy and her other superpowered friend, Eliza Dushku's Faith, were out slaying vampires when Faith messed up and rammed her wooden stake into the heart of a guy who turned out to be human.

He died instantly in a death scene that was as unsettling as it was unexpected. And in tonight's episode the girls are still trying to deal with it. Faith's in denial while Buffy is haunted by what happened.

(BEGIN AUDIO CLIP -- SCENE FROM WB TELEVISION SERIES "BUFFY THE VAMPIRE SLAYER")

ELIZA DUSHKU, ACTRESS: Buffy, I'm not going to see anything. I missed the mark last night, and I'm sorry about the guy. I really am. But it happens. Anyways, how many people do you think we've saved by now? Thousands? And didn't you stop the world from ending? Because in my book that puts you and me in the plus column.

SARAH MICHELLE GELLAR, ACTRESS: We help people. It doesn't mean we can do whatever we want.

DUSHKU: Why not? The guy I offed was no Ghandi. I mean we just saw it, he was mixed in dirty dealings.

GELLAR: Maybe. But what if he was coming to us for help?

DUSHKU: What if he was? You're still not seeing the big picture, B. Something made us different. We're warriors. We were built to kill.

GELLAR: To kill demons. That does not mean that we get to pass judgment on people like we're better than everybody else.

DUSHKU: We are better. That's right, better. People need us to survive. In the balance, nobody is going to cry over some random bystander who got caught in the crossfire.

GELLAR: I am.

DUSHKU: That's your loss.

BIANCULLI: Because of scenes like this, "Buffy" rounds out my top five. So that's it: two law shows, two cop shows, and a show about not so fearless vampire killers. There may not be a lot of variety, but there sure is a lot of quality.

GROSS: David Bianculli is TV critic for the "New York Daily News."

I'm Terry Gross.

This is a rush transcript. This copy may not
be in its final form and may be updated.

TO PURCHASE AN AUDIOTAPE OF THIS PIECE, PLEASE CALL 888-NPR-NEWS

Dateline: Terry Gross, Washington, DC
Guest: David Bianculli
High: TV critic David Bianculli gives us his top five favorite TV dramas.
Spec: Television and Radio; Lifestyle' Culture; Entertainment; David Bianculli

Please note, this is not the final feed of record
Copy: Content and programming copyright 1999 WHYY, Inc. All rights reserved. Transcribed by FDCH, Inc. under license from WHYY, Inc. Formatting copyright 1999 FDCH, Inc. All rights reserved. No quotes from the materials contained herein may be used in any media without attribution to WHYY, Inc. This transcript may not be reproduced in whole or in part without prior written permission.
End-Story: David Bianculli
Transcripts are created on a rush deadline, and accuracy and availability may vary. This text may not be in its final form and may be updated or revised in the future. Please be aware that the authoritative record of Fresh Air interviews and reviews are the audio recordings of each segment.

You May Also like

Did you know you can create a shareable playlist?

Advertisement

Recently on Fresh Air Available to Play on NPR

52:30

Daughter of Warhol star looks back on a bohemian childhood in the Chelsea Hotel

Alexandra Auder's mother, Viva, was one of Andy Warhol's muses. Growing up in Warhol's orbit meant Auder's childhood was an unusual one. For several years, Viva, Auder and Auder's younger half-sister, Gaby Hoffmann, lived in the Chelsea Hotel in Manhattan. It was was famous for having been home to Leonard Cohen, Dylan Thomas, Virgil Thomson, and Bob Dylan, among others.

43:04

This fake 'Jury Duty' really put James Marsden's improv chops on trial

In the series Jury Duty, a solar contractor named Ronald Gladden has agreed to participate in what he believes is a documentary about the experience of being a juror--but what Ronald doesn't know is that the whole thing is fake.

08:26

This Romanian film about immigration and vanishing jobs hits close to home

R.M.N. is based on an actual 2020 event in Ditr─âu, Romania, where 1,800 villagers voted to expel three Sri Lankans who worked at their local bakery.

There are more than 22,000 Fresh Air segments.

Let us help you find exactly what you want to hear.
Just play me something
Your Queue

Would you like to make a playlist based on your queue?

Generate & Share View/Edit Your Queue