New Treatments Give Hope To Cancer Patients The announcement of new personalized cancer therapies offers signs of hope — but no cure yet — to many suffering from the disease. Two treatment options may prolong the lives of patients with melanoma. There are also hormone-blocking pills that may prevent breast cancer in women at high risk.
NPR logo

New Treatments Give Hope To Cancer Patients

  • Download
  • <iframe src="" width="100%" height="290" frameborder="0" scrolling="no" title="NPR embedded audio player">
  • Transcript
New Treatments Give Hope To Cancer Patients

New Treatments Give Hope To Cancer Patients

New Treatments Give Hope To Cancer Patients

  • Download
  • <iframe src="" width="100%" height="290" frameborder="0" scrolling="no" title="NPR embedded audio player">
  • Transcript

The announcement of new personalized cancer therapies offers signs of hope — but no cure yet — to many suffering from the disease. Two treatment options may prolong the lives of patients with melanoma. There are also hormone-blocking pills that may prevent breast cancer in women at high risk.


Matthew Herper, senior editor, Forbes
Dr. Ora Gordon, director, GenRISK Adult Genetics program

NEAL CONAN, host: This is TALK OF THE NATION. I'm Neal Conan in Washington. Big news last week from the annual conference of cancer doctors in Chicago. The American Society for Clinical Oncology heard about new, personalized therapies that promise hope. New treatments for melanoma and lung cancer promise to extend the lives of patients with a specific gene defect or a specific type of tumor.

Advancements in prevention of breast cancer for millions of women at high risk comes in the form of a hormone-blocking pill. While studies back the positive effect of the new drugs, many cancer experts question their cost and the looming difficulties involved in creating and testing individualized drugs in the future.

Cancer patients, what do you want to know about these new advances? Our phone number is 800-989-8255. Email You can also join the conversation on our website. That's at Click on TALK OF THE NATION.

Later in the program, we want to hear from those of you who have ever co-signed a loan. How'd that work out? Email us now. The address again,

But first, the war on cancer. Matthew Herper joins us from our bureau in New York. He's senior editor at Forbes magazine, where he covers science and medicine, and it's nice to have you with us today.

MATTHEW HERPER (Forbes Magazine): Thank you so much for having me.

CONAN: And you know better than I, over the past several years, we've heard a lot about promising breakthroughs on cancer, which turn out to be less than - less dramatic than promised. Should we be cautious about the news from Chicago last week?

HERPER: We should. I mean, we've been through several years of ASCOs. I've been going to this meeting for a long time. And we've been through several years where the level of innovation hasn't been what we would have hoped, say eight or nine years ago. I mean, there was a period where there was a drug called Gleevec that really, really helped in a certain type of leukemia by hitting a very particular mutation. And there was a lot of hope that we were starting to kind of crack the code, and it's been harder than people thought.

CONAN: Harder than people thought, in part, and this was interesting to read, in part because there are smart cancers and dumb cancers.

HERPER: Yeah, there was an amazing presentation by the current president of ASCO, which is a one-year position held by a top academic doctor. This guy's name is George Sledge. And he went through what we're going to have to do in order to make personalized medicine work.

I mean, one of the biggest stories in medicine right now is that sequencing DNA, which remember cost $3 billion when Craig Venter did it 10 years ago...

CONAN: For himself, yeah.

HERPER: For himself. Now, we're in kind of the $5,000 range, and the ability to do that is really promising in cancer because you can start finding the particular mutations that matter for - that make someone respond to a drug. And we have some examples. One of them was a big melanoma drug. But Dr. Sledge went through how, you know, there are these - there are dumb cancers, like the one that Gleevec, that wonder drug I was just talking about, targeted. And then there are smart cancers like melanoma.

And we had this - there was this wonderful melanoma drug at the meeting this year, and Dr. Sledge put up this fantastic, horrifying image of a patient with melanoma who received that drug. Their torso was all lumpy with tumors. They all went away, and they all came back.

You know, really pretty - it's, you know, it's an Indian giver. The drug is really a breakthrough. It really does help patients, but it's still smarter than we are.

CONAN: So a dumb cancer like the kind of...

HERPER: CML leukemia, yes.

CONAN: So it didn't adapt. It was a low-hanging fruit, if you will.

HERPER: Right. What happened is there was one gene that went wrong to cause the cancer, and all you had to do was fix that gene, and everything else that was wrong got fixed. The body took care of it.

But I mean, you think of a cancer that's caused by smoking. You know, that's caused by that cigarette smoke damaging the cells in your lungs and their DNA over years. And lots of things go wrong, and they kind of pile up. And you can't just pull one switch and fix it.

And so how do you turn all those switches at once? How do you figure out how to turn all those switches at once? It's like you're in a control room, and you have to fix, and you have to get exactly the right combination, or it's not going to work. It's much harder.

CONAN: I was astonished to read that - I think they said one mutation per every three cigarettes you smoked?

HERPER: Yes, it's pretty stunning, actually.

CONAN: And so if you smoked a pack a day for 20 years, you're going to have quite a case of cancer if you develop it.

HERPER: I mean, in a lot of cancers, smoking is - in lung cancer, the targeted drugs are tending to work best in people who didn't smoke and have different kinds of mutation. And that goes for Tarceva and a new Pfizer drug called Crizotinib, which is one of these gene-targeted drugs.

And it's also true in head and neck cancer. I mean, we're finding out that in the past decade or so, most head and neck cancers are being caused by HPV, the same virus that causes cervical cancer. It's sexually transmitted and happens mostly in men, heterosexual men, and those cancers are much easier to treat than the ones that are caused by smoking.

And even if you have the HPV-caused cancer, and you smoke, that's a risk factor that makes your prognosis worse.

CONAN: So the good news is that you - we have the promise of individualized, genetically individualized drugs. The bad news is: Boy, that's not going to be easy.

HERPER: Right, it's very, very difficult to make genetically individualized drugs because you have to - especially if they have to work in combination. You go from having to screen through 14 patients for testing for everyone you enter into a clinical trial to screen through 150.

It's also very, very - it's more difficult to invent these drugs, and one thing we're finding is that these drugs are coming to the market at very high prices because of the way our system currently works. You know, I mean, new cancer drugs seem to cost somewhere between 70,000 and $100,000 per patient. They can be more for very rare cancers. So it's costly.

And there are all these logistical hurdles of how do you sequence the cancer, which is a different genome than yours. It's a sequence of cancer in yourself. How do you - how do you get patients who have a particular mutation into the right trial? You have to - instead of saying I'm going to do a clinical trial, and I'm going to search for the people for that clinical trial, you have to be - have a whole bunch of clinical trials so when you find somebody, you have a trial to put them in. Otherwise, you're going to be not testing enough patients.

And we just aren't set up to do this. I mean, this is an electronic health record problem. It's a computational problem, and it's a technology problem.

CONAN: Well, joining us now from our studios at NPR West is Dr. Ora Gordon. She's director of GenRISK Adult Genetics Program and genetics director of the Wasserman Breast Cancer Risk Reduction at Cedars-Sinai Hospital in Los Angeles, and it's nice to have you with us today.

Dr. ORA GORDON: My pleasure to join you.

CONAN: And do you expect that someday, in your lifetime, you're going to begin someone's cancer treatment by looking at their genome on a thumb drive?

GORDON: Well, in some ways, we're already starting down that road. In my work through the Wasserman Prevention Program and the bigger Ocean Cancer Center, you know, there are two approaches. One is prevention, primary prevention and what is the genetics of risk.

Now, certainly we have a good understanding of the very high-risk genes, but the genomic risk, this idea of these small influences in one person versus another that make them more or less vulnerable to any form of cancer or perhaps to any therapy, is where we're really focusing on currently.

CONAN: So that is part of your practice right now?

GORDON: It is. There are a few commercially available tests for genomic risks, for cancer and other kinds of adult chronic diseases. But what we're really trying to do is understand, on a bigger level, how does that interact with what's known to be the risk factors.

You referred to the study that was released last week in terms of the Exemestane, this drug that is used for the prevention of recurrence of breast cancer and now in this trial for primary prevention in all women who are at elevated risk. But what's the biology or the genetics of all of those women? Are they all likely or not likely to respond?

This is sort of our hopes of where we're going to go, which may turn out to be easier than targeting the cancer itself, which as already reviewed, is so much a part of these mutations that are acquired in the tumor. So that's not what you've inherited. It's the tumor itself having gone awry and continuing to change and outsmart the drugs that we have to offer it.

CONAN: So best to stop it before it gets to the tumor stage.

GORDON: That's certainly my - that's my idea.

CONAN: And is that going to be - you're just suggesting that might be a little easier than dealing with the tumor but not a piece of cake, either, I suspect.

GORDON: Without question. In fact, easy is not the right word at all. The human genome sequencing now, we're really moving towards - as spoken, you know, that the cost has come down, the technology has improved so much so that now we have these massive amounts of data that we can compare one person to another. But really the interpretation at this point is very limited.

We don't know - we can see variations from one large group of people to another and say there's a difference in risk for breast cancer, for example, but we don't have the full answer. We still can't account for why, you know, Sally gets breast cancer, and Jane does not.

CONAN: And I just wonder how much your knowledge base has changed since you graduated. You know, since you took on your specialty, you've had to master areas of information technology that you probably never imagined when you graduated.

GORDON: That's absolutely correct.

CONAN: It's a whole - and Matthew Herper, there's - you're talking about a whole field of medicine that is going to have to become, well, computer-savvy is not quite the right word. There...

HERPER: Well, it's more than computer-savvy. You have to become computational scientists and biologists in addition to doctors. And one thing I wonder about on prevention, I mean, having covered the pharmaceutical industry, prevention was a big topic of focus when I started covering the industry about 10 years ago. It's not now, because the only way people are making money is with these very expensive cancer drugs.

So we're not seeing preventative tests because it's too hard to run the clinical trials. We're not seeing preventative medicines. I mean, I wonder with Exemestane, that's a drug that is likely to face patent expiration. It hasn't been that big for Pfizer, and it hasn't sold that well in reducing risk of second breast cancers.

So will women use it? I mean, there's not going to be that kind of market push that we've seen with, you know, Lipitor and Zocor and the cholesterol drugs.

CONAN: Dr. Gordon?

GORDON: Well, I think there are two issues. You know, one is I agree completely there has not been enough industry-related incentive to come up with new preventive medications, especially perhaps low-tech ones, which may be hormonal modulators that are plant-based and therefore not likely to be lucrative.

But I don't think that it's not a focus of health care and the priority of the National Cancer Institute, for example, in terms of really targeting prevention.

CONAN: We're talking about new drugs and targeted treatments for cancer. If you have been diagnosed with cancer, what do you want to know about these new advances? Give us a call, 800-989-8255. Email us, Stay with us. I'm Neal Conan. It's the TALK OF THE NATION, from NPR News.


CONAN: This is TALK OF THE NATION from NPR News. I'm Neal Conan, in Washington. A new group of cancer drugs promises to target specific genes in individual tumors or patients. The result: treatments that can prevent some cancers or extend the lives of patients with other forms of the disease.

Personalized medicine is changing the way researchers approach cancer, thanks to advances in genetics and technology, though some caution the reality of this research may never quite match the promise.

Cancer patients, what do you want to know about these new advances? 800-989-8255. Email us: You can also join the conversation on our website. That's at Click on TALK OF THE NATION.

Our guests are Matthew Herper, senior editor at Forbes, where he covers science and medicine. He attended the 2011 American Society of Clinical Oncology conference. We've posted a link to his coverage of those new treatments at our website. Again, that's Click on TALK OF THE NATION. Also Dr. Ora Gordon, who serves as genetics director of the Wasserman Breast Cancer Risk Reduction Program. She wrote the book "Positive Results: Making the Best Decisions when You're at High Risk for Breast or Ovarian Cancer."

We have this email from Sue: I was listening to a doctor the other day who was singing the praises of prophylactic pharmaceuticals, including a drug that might protect women over 60 from breast cancer. The drug had some serious side effects: vision problems, kidney, liver damage, et cetera, and those were just the ones mentioned. And the odds of a woman over 60 being diagnosed with breast cancer is 1.6 percent. I'll take my chances with those odds and save my eyes and my internal organs from the toxins and expense of these drugs.

Dr. Gordon, is that the drug we're talking about?

GORDON: It sounds like it, although I think she's mixed a little bit in terms of her - the risk and the side-effect profiles. But yes, the two drugs, you know, the drugs that are currently available are tamoxifen and Evista, which do have a pretty long list of potential side effects, including problems with the eyes and even cancer of the uterus.

But the Exemestane, that's a new drug, is very well-tolerated overall. The risk in a woman over 60, her annual risk for breast cancer is about .6 percent. And she might even say that's even lower and even less inclined to take a medication. But there has - the evidence from this study shows a very substantial risk reduction, 65 percent risk reduction in the women in a relatively short period of time of those getting cancer who took the medicine, who didn't. And the side effects for people taking placebo versus those who took the medication were about matched.

CONAN: Placebo, sugar pill.

GORDON: That's right, a sugar pill. So they complained of the same thing: body aches, hot flashes, not feeling so good.

CONAN: That's I think what we all complain about.


CONAN: Let's see if we can get a caller in. This is Victoria, Victoria with us from Danville in California.

VICTORIA (Caller): Hi. I was diagnosed with breast cancer, fortunately stage one, in April of 2009, had the radiation, did not have to do chemo because I had an Oncotype DX test that was very low. But I've been on tamoxifen for two years now. I'm post-menopausal. I tried one of the aromatase inhibitors. There's, I think, three now. And I tried the Femara, which was supposed to have the least amount of side effects, and it crippled me.

I could not get up out of bed. I could not walk. And I'm very healthy otherwise and relatively young. I'm 55 years old. So I went back on the tamoxifen. My question is why these wonderful drugs that help prevent recurrence - and I'm talking about treatment now, as opposed to prevention - why the side effects are so severe.

And the oncologists, all of them from I can gather - or most of them, I shouldn't generalize - basically say: Oh, yes, premature cataracts, very common. But they're my eyes. There are humans here who are suffering with quality-of-life issues, and the oncologists, who I see as sort of statisticians, are just sort of going: Well, you kind of have to suck it up.

And I've had - and I'm now back on the tamoxifen. I have another three years to go on this, and it's severe joint pain, hot flashes, the previously mentioned premature cataracts. You know - and I have it pretty easy, from what I've read online.

CONAN: Dr. Gordon?

GORDON: Well, the caller - certainly any one individual, it's the hardest thing in medicine is, you know, what do we apply to the group, and what does one person experience? The side effects that you had on Femara are in the extreme in terms of overall, but very important, obviously.

Part of this whole idea of personalized medicine and genomics and trying to understand who might have a hypersensitivity or an extreme sensitivity to any one medication, perhaps your body metabolizes it in a way that would double the toxic side effects.

And although we've made fits and starts in trying to better understand that, and in a few drugs we have a very clear path, for the most part, we really can't determine ahead of time who is most likely to benefit from any one drug, whether it be for prevention or for treatment.

HERPER: If I could just add something...

VICTORIA: But then...

CONAN: Hold on, Matt. Victoria, hold on just a second. Matthew Herper?

HERPER: The other thing to remember is that drug companies did think that tamoxifen wasn't - was a drug they could improve on, and that's why we have the aromatase inhibiters. And inventing a new drug is a lot harder than I think people think.

I mean, aside from the numbers that get thrown about - how much it costs, a billion dollars or - I mean, only one of every 11 or so drugs that goes into clinical trials makes it. So the reality is that getting rid of those side effects is really, really tough, which is why we have all these discussions about risk and benefit.

CONAN: Victoria, I'm sorry.

VICTORIA: Well, what I was going to then say was is that it would appear that the only way I can combat these particular side effects is with more prescription drugs, which carry their own. So I'm sort of on the side-effect train.

CONAN: And this is a complaint, Dr. Gordon, that I think is not Victoria's alone, that it seems to be a revolving door that there's one and then another to ameliorate the effects of that, and then another to ameliorate the effects of that, and pretty soon, you're taking 25 tablets.

GORDON: Yeah, that is a problem. And, in fact, sometimes we give medication - for example with tamoxifen, if people have side effects, we may give them another medication, which is in the antidepressant class of medications, to help combat their hot flashes, which may in fact inactivate the tamoxifen. So it really is pretty challenging.

VICTORIA: Okay, well, that sounds like basically I've gotten some questions answered. I sort of knew what the answer was going to be. And I guess I'm just going to have to suck it up, yeah?

CONAN: Victoria, as the civilian here, I will say probably that's the answer, yeah.

VICTORIA: Okay, well, thank you very much. I appreciate it.

CONAN: Good luck with it. I know it's not going to be easy.

VICTORIA: Okay, thank you.

CONAN: Here's an email, this from Brad, I think his name is, in Emmett, Idaho: Three months ago today, my father died from a glioblastoma brain cancer. Going through that process and learning more about the whole world of cancer taught me how much is really not known about the cause and cure of cancer after decades of research.

Is there any progress being made to shift some of the massive amount of money currently being spent on drugs to lifestyle prevention measures such as diet and environmental exposures? And Matthew Herper, you were talking about that earlier, that there was less emphasis on preventive therapies, but what about these other practices?

HERPER: Well, I would say the answer is probably not really. I mean, the way we really fund drug development is through the stock market, as much as through the NIH. I mean, you look at the huge amounts of money spent by pharmaceutical companies. I mean, Pfizer alone is seven or $8 billion.

So I - that and their interest in a product, I would personally wonder whether we could - and this is an idea I'm stealing from a Nobel Prize-winner named Lee Hartwell, who is - who founded some cancer companies, was at the Fred Hutchinson Cancer Institute.

And he told me once that he thought that we'd be a lot better off if we were developing new diagnostics to detect cancer earlier and to figure out - to match drugs to patients instead of spending so much focus on finding new targeted agents.

And I always wonder about that, because the development - the amount of money you make creating a diagnostic test isn't nearly as much as for a cancer drug like, say, Avastin or Rituxan, which are the really big sellers now.

CONAN: And you say that, yet we hear that the guy who devised the PSA test, I think every man now takes once a year or so, wishes he never had.

HERPER: Well, it's not - the problem with the PSA tests, and I've heard this argument from so many top cancer doctors, it's not a very good predictor of who's going to get prostate cancer, and it's a very slow cancer. So there's the risk of over-treatment.

It's a very difficult problem. I mean, it's the - it's what people are actually struggling with, with all these directions from a genetic test: When is it too much information? When are you better off not knowing?

CONAN: Is there any point, Dr. Gordon, in which people are better off not knowing?

GORDON: Well. I think the current direct-to-consumer market is - there's still much that remains in terms of really what we know, and even the interpretation that we can get from the information that's presented.

I don't know whether there's ever a point that there's too much information that's, you know, not good, except for that if you don't have an actionable, you know, something you can do for it, or it's conflicting with other data, and then you're left with, you know, who do you pull for the third straw, I think that becomes really very problematic.

CONAN: Let's go to Larry, Larry with us from Phoenix.

LARRY: Hi. I have a question for your panel. I recently became aware of a term, number needed to treat, in connection with my mother-in-law being diagnosed with cancer. And we're shocked to find the degree to which that term is not generally - or the information is not generally provided to patients. And that my understanding is it simply means that you might have to administer a drug to up to 100 or more people in order to get the intended outcome in one. And I'm curious as to your panel's comment on both the concept and the degree to which the public is not making informed choices by reason of their not being aware of this concept.

CONAN: Matthew Herper, are you familiar with the number needed to treat?

HERPER: I'm very familiar with the term, number needed to treat. From my perspective, this is actually a tough one, because I'm not sure that number needed to treat is necessarily better than, say, relatively risk. I think that they can both be used as kind of as you want them to be used.

I mean, I've seen a lot of people - sometimes, if you tell people that, you know, you tell something, this increases your survival 60 percent - and I'm just pulling numbers out of a hat - but the number needed to treat is, you know, 50 or 100, the number needed to treat has - well, it's a lot of people and it's a big decrease in risk. Well, you - how do you - those - I don't think people are good at judging either number.

LARRY: If I can just quickly follow on question, then I'll get off the line to listen to the answer. I would respectfully disagree as a lay person. If you tell me that on the placebo group, one person had a favorable outcome with no drug, and two people have an outcome that was favorable with the prescribed drug, but it took 200 people in the test to get one additional favorable outcome. And so that means it increased favorable outcomes from one to two. And in addition to that, all of the side-effect profiles hit the entire population of 200, potentially. And so there's the number needed to harm concept as well. Having said that, I'll get off the line and listen to your answer on the radio.

CONAN: All right, Larry. Thank you.

HERPER: The number needed - that's absolutely true, which is why it's important that your outcome is something you actually care about, which is one of the main things one looks at when looking at, say, biotech companies. Are they actually selling something? But if you're - if the - I mean, if that one outcome is death, might that be worth it? I mean, at those numbers we just gave.

GORDON: Right.

CONAN: We're talking with Doctor Ora Gordon of the GenRISK Adult Genetics Programs and genetics director of the Wasserman Breast Cancer Risk Reduction Program, and author of "Positive Results: Making the Best Decisions When You're at High Risk for Breast or Ovarian Cancer." Also with us, Matthew Herper, senior editor at Forbes magazine, covering science and medicine and wrote a series of blog post treatments, "Cancer's New Era of Promise and Chaos." There's a link to those at our website. Go to, click on TALK OF THE NATION. And this is TALK OF THE NATION, coming to you from NPR News.

And, Doctor Gordon, just to follow up on that last point, sometimes, it seems that the benefit is extension of a life by a month, or six weeks or eight weeks. Sometimes, as you say, the risk is death. These are terrible things to conjure with and these are very disturbing things to talk about with patients.

GORDON: They are. And when you look at these studies, particularly in individuals who have advanced cancers, who have been treated numerous other therapies and the, you know, splash on the headlines is this tremendous, you know, difference in benefit. And then you look at the numbers and it says it's, you know, five-month increase in overall survival. And that seems rather grim. So I think that it's really a challenge to apply it.

In reference to the caller, for example, when talking about, like this prevention - the numbers needed to treat with the Exemestane was estimated at 25 or so to treat to get - to prevent one breast cancer. So, again, it is very much a balance between how many people will not likely get benefit but not likely be harmed, over the burden. And the death is the burden of not getting response to therapy. I don't think any drug with the risk of death being as a consequence of therapy is going to go to market.

CONAN: Here's an email from Maria in Boise. Can the commentators talk about how research is funded? My wife recently passed away from NSC lung cancer. We were astounded at the statistics regarding the death rate of lung cancer. Number one cancer killer of women, nearly twice as many as breast cancers, versus funding levels for research and treatment. And, Doctor Gordon, you're a specialist on breast cancer. Can you address that?

GORDON: Yeah, lung cancer in women has definitely been an overlooked area. There's now a great deal more attention, focusing on that, particularly, you know, lung cancer in nonsmoking women. And it's probably a very distinct biology, a very distinct genetic susceptibility in those individuals. And some of the targeted therapies that were also discussed earlier, in a small fraction of those, may be really home runs in terms of response. But, again, we won't know if it lasts.

CONAN: And, Matthew Herper, you talked about research really being driven by the stock market.

HERPER: Well - and that's not - that's resulted in some pretty interesting lung cancer drugs. I mean, again, it's been tough. I mean, I was talking to Mark Kris, who's a well-known researcher in that area - and he was saying that, you know, when we add Tarceva and Crizotinib, which is this experimental Pfizer drug not on the market, there's actually - for a lot of those people, there is - these start to add up as you get more of them. But it's been - I mean, the drug industry has been going through an innovation drought for the entire time I've been covering them. I mean, it's been very hard to get new products to market. So, you know, that means that for any given cancer, there haven't been that many drugs.

CONAN: It was also interesting to read your conclusion, that with individualized information from our genomes, effectively every cancer will be a rare cancer.

HERPER: Every cancer will be an orphan disease is something I keep hearing. And, you know, that's kind of scary when each drug is costing $100,000. I mean, obviously, we do need to try to find other answers for how to pay for this. But one thing that was - the head of cancer research at Merck, Gary Gilliland, told me that he doesn't want drugs anymore. As you're picking your patients with these new diagnostics, one of the big benefits is he's not - no longer looking for drugs where there's a small benefit. He wants a big benefit. So that's good news.

CONAN: That's good news. We'll look forward to silver bullets next year.

HERPER: Silver shotguns.

CONAN: Silver shotguns. Yes, of course. I misspoke. Matthew Herper, thank you very much for your time today.

HERPER: Thank you.

CONAN: And, Dr. Gordon, we appreciate your coming in to speak with us.

GORDON: My pleasure.

CONAN: Matthew Herper joined us from our bureau in New York. Dr. Gordon was at NPR West in Culver City, California. Coming up, don't ever sign on a loan, ever. Megan McArdle makes the argument in The Atlantic. She joins us next why - to explain why. Stay with us. It's TALK OF THE NATION from NPR News.

Copyright © 2011 NPR. All rights reserved. Visit our website terms of use and permissions pages at for further information.

NPR transcripts are created on a rush deadline by Verb8tm, Inc., an NPR contractor, and produced using a proprietary transcription process developed with NPR. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record.

Read Matthew Herper's Series, "Cancer's New Era Of Promise And Chaos"