Why Choose Alternative Cancer Treatments (27b)

Why We’re Losing The War on Cancer [and How to Win It]

by Clifton Leaf, Fortune Magazine, March 22, 2004

ctd. from first page

“WE HAVE A SHORTAGE OF GOOD IDEAS”

IT IS ONE OF THE MANY chicken-and-egg questions bedeviling the cancer culture. Which came first: the FDA’s imperfect standards for judging drugs or the pharmaceutical companies’ imperfect models for testing them?

The riddle is applicable not just to early drug development, in which flawed animal models fool bench scientists into thinking their new compounds will wallop tumors in humans. It comes up, with far more important ramifications, in the last stage of human testing, when the FDA is looking for signs that a new drug is actually helping the patients who are taking it. In this case, the faulty model is called tumor regression. It is exciting to see a tumor shrink in mouse or man and know that a drug is doing that. A shrinking tumor is intuitively a good thing. So it is no surprise that it’s one of the key endpoints, or goals, in most clinical trials. That’s in no small part because it is a measurable goal: We can see it happening. (When you read the word “response” in a newspaper story about some exciting new cancer drug, tumor shrinkage is what it’s talking about.)

“People obsessed with cures, cures, cures are being— I hate to use the word—selfish by ignoring what could be done in terms of prevention.”

But like the mouse, tumor regression by itself is actually a lousy predictor for the progression of disease. Oncologists can often shrink a tumor with chemo and radiotherapy. That sometimes makes the cancer easier to remove surgically. If not, it still may buy a little time. However, if the doctors don’t get every rotten cell, the sad truth is that the regression is not likely to improve the person’s chances of survival.

That’s because when most malignant solid tumors are diagnosed, they are typically quite large already—the size of a grape, perhaps, with more than a billion cells in the tumor mass. By the time it’s discovered, there is a strong chance that some of those cells have already broken off from the initial tumor and are on their way to another part of the body. This is called metastasis.

Most of those cells will not take root in another tissue or organ: A metastasizing cell has a very uphill battle to survive once it enters the violent churn of the bloodstream. But the process has begun— and with a billion cells dividing like there’s no tomorrow, an ever-growing number of metastases will try to make the journey. Inevitably, some will succeed.

In the end, it is not localized tumors that kill people with cancer; it is the process of metastasis—an incredible 90% of the time. Aggressive cells spread to the bones, liver, lungs, brain, or other vital areas, wreaking havoc. So you’d think that cancer researchers would have been bearing down on this insidious phenomenon for years, intently studying the intricate mechanisms of invasion. Hardly. According to a FORTUNE examination of NCI grants going back to 1972, less than 0.5% of study proposals focused primarily on metastasis—trying to understand, for instance, its role in a specific cancer (e.g., breast, prostate) or just the process itself. Of nearly 8,900 NCI grant proposals awarded last year, 92% didn’t even mention the word metastasis.

One accomplished researcher sent an elegant proposal into the NCI two years ago to study the epigenetics (changes in normal gene function) of metastases vs. primary tumors. It’s now in its third resubmission, he says. “I mean, there is nothing known about that. But somehow I can’t interest people in funding this!”

M.D. Anderson’s Josh Fidler suggests that metastasis is getting short shrift simply because “it’s tough. Okay? And individuals are not rewarded for doing tough things.” Grant reviewers, he adds, “are more comfortable with the focused. Here’s an antibody I will use, and here’s blah-blah-blah-blah, and then I get the money.”

Metastasis, on the other hand, is a big idea—an organism-wide phenomenon that may involve dozens of processes. It’s hard to do replicable experiments when there are that many variables. But that’s the kind of research we need. Instead, says Weinberg, researchers opt for more straightforward experiments that generate plenty of reproducible results. Unfortunately, he says,“the accumulation of data gives people the illusion they’ve done something meaningful.”

That drive to accumulate data also goes to the heart of the regulatory process for drug development. The FDA’s mandate is to make sure that a drug is safe and that it works before allowing its sale to the public. Thus, the regulators need to see hard data showing that a drug has had some effect in testing. However, it’s hard to see “activity” in preventing something from happening in the first place. There are probably good biomarkers—proteins, perhaps, circulating in the body—that can tell us that cancer cells have begun the process of spreading to other tissues. As of yet, though, we don’t know what they are.

So pharma companies, quite naturally, don’t concentrate on solving the problem of metastasis (the thing that kills people); they focus on devising drugs that shrink tumors (the things that don’t).

Dozens of these drugs get approved anyway. At the same time, many don’t—and the FDA is invariably blamed for holding up the War on Cancer. The fault, however, is less the umpire’s than the players’. That’s because many tumor-shrinking drugs simply don’t perform much better than the standard treatments. Or as Rick Pazdur, director of oncology drugs for the FDA, puts it, “It’s efficacy, stupid! One of the major problems that we have is dealing with this meager degree of efficacy.” When it’s clear that something is working, the agency is generally quick to give it priority review and/or accelerated approval, two mechanisms that speed up the regulatory process for compounds aimed at life-threatening diseases. “We have a shortage of good ideas that are likely to work,” agrees Bruce Johnson, a Dana-Farber oncologist who runs lung-cancer research for institutions affiliated with the Harvard Medical School, a huge partnership that includes Massachusetts General Hospital, Brigham and Women’s Cancer Center, and others.

That is also the devastating conclusion of a major study published last August in the British Medical Journal. Two Italian pharmacologists pored over the results of trials of 12 new anticancer drugs that had been approved for the European market from 1995 to 2000, and compared them with standard treatments for their respective diseases. The researchers could find no substantial advantages— no improved survival, no better quality of life, no added safety— with any of the new agents. All of them, though, were several times more expensive than the old drugs. In one case, the price was 350 times higher.

WHY THE NEW DRUGS DISAPPOINT

FLAWED MODELS FOR DRUG development. Obsession with tumor shrinkage. Focus on individual cellular mechanisms to the near exclusion of what’s happening in the organism as a whole. All these failures come to a head in the clinical trial—a rigidly controlled, three-phase system for testing new drugs and other medical procedures in humans. The process remains the only way to get from research to drug approval—and yet it is hard to find anyone in the cancer community who isn’t maddeningly frustrated by it.

In February 2003 a blue-ribbon panel of cancer-center directors concluded that clinical trials are “long, arduous,” and burdened with regulation; without major change and better resources, the panel concluded, the “system is likely to remain inefficient, unresponsive, and unduly expensive.”

All that patients know is that the process has little to offer them. Witness the fact that a stunning 97% of adults with cancer don’t bother to participate.

There are two major problems with clinical trials. The first is that their duration and cost mean that drug companies—which sponsor the vast majority of such trials—have an overwhelming incentive to test compounds that are likely to win FDA approval. After all, they are public companies by and large, with shareholders demanding a return on investment. So the companies focus not on breakthrough treatments but on incremental improvements to existing classes of drugs. The process does not encourage risk taking or entrepreneurial approaches to drug discovery. It does not encourage brave new thinking. Not when a drug typically takes 12 to 14 years to develop. And not with $802 million—that’s the oft-cited cost of developing a drug—on the line.

What’s more, the system essentially forces companies to test the most promising new compounds on the sickest patients—where it is easier to see some activity (like shrinking tumors) but almost impossible to cure people. At that point the disease has typically spread too far and the tumors have become too ridden with genetic mutations. Thus drugs that might have worked well in earlier-stage patients often never get the chance to prove it. (As you’ll see, that may be a huge factor in the disappointing response so far of one class of promising new drugs.)

The second problem is even bigger: Clinical trials are focused on the wrong goal—on doing “proper” science rather than saving lives. It is not that they provide bad care—patients in trials are treated especially well. But the trials’ very reason for being is to test a hypothesis: Is treatment X better than treatment Y? And sometimes—too often, sadly—the information generated by this tortuously long process doesn’t much matter. If you’ve spent ten-plus years to discover that a new drug shrinks a tumor by an average of 10% more than the existing standard of care, how many people have you really helped?

Take two drugs approved in February for cancer of the colon and rectum: Erbitux and Avastin. In each case it took many months just to enroll the necessary number of patients in clinical trials. Participating doctors then had to administer the drugs according to often arduous preset protocols, collecting reams of data along the way. (ImClone’s well-known troubles with the FDA occurred because it had not set up its trials properly.)

And here’s what clinicians learned after years of testing. When Avastin was added to the standard chemotherapy regimen, the combination managed to extend the lives of some 400 patients with terminal colorectal cancer by a median 4.7 months. (A previous trial of the drug on breast cancer patients failed.) Oncologists consider the gain substantial, considering that those in advanced stages of the disease typically live less than 16 months.

And Erbitux? Although it did indeed shrink tumors, it has not been shown to prolong patients’ lives at all. Some certainly have fared well on the drug, but survival on average for the groups studied didn’t change. Still, Erbitux was approved for use primarily in “third line” therapy, after every other accepted treatment has failed. A weekly dose costs $2,400.

Remember, it took several years and the participation of thousands of patients in three stages of testing, tons of data, and huge expense to find out what the clinicians and researchers already knew in the earliest stage of human testing: Neither drug will save more than a handful of the 57,000 people who will die of colorectal cancer this year.

You could say the same for AstraZeneca’s Iressa, another in the new class of biological wonder drugs—compounds specifically “targeted” to disrupt the molecular signals in a cancer cell. Not a single controlled trial has shown Iressa to have a major patient benefit such as the easing of symptoms or improved survival—a fact that the company’s upbeat press releases admit as if it were legal boilerplate. Even so, the FDA okayed the pill last year for last-ditch use against a type of lung cancer, citing the fact that it had shrunk tumors in 10% of patients studied.

“Very smart people, with a lot of money, have done trials of over 10,000 patients around the world—testing these new molecular targeted drugs,” says Dana-Farber’s Bruce Johnson. “AstraZeneca tested Iressa. Isis Pharmaceuticals and Eli Lilly tested a compound called Isis 3521. Several different companies ended up investing tens of millions of dollars, and all came up with a big goose egg.”

The one targeted drug that clearly isn’t a goose egg is Novartis’s Gleevec, which has been shown to save lives as well as stifle tumors. The drug has a dramatic effect on an uncommon kind of leukemia called CML and an even more rare stomach cancer named GIST. Early reports say it also seems to work, in varying degrees, in up to three other cancers. Gleevec’s success has been held out as the “proof of principle” that the strategy we’ve followed in the War on Cancer all these years has been right.

But not even Gleevec is what it seems. CML is not a complicated cancer: In it, a single gene mutation causes a critical signaling mechanism to go awry; Gleevec ingeniously interrupts that deadly signal. Most common cancers have perhaps as many as five to ten different things going wrong. Second, even “simple” cancers get smarter: The malignant cells long exposed to the drug (which must be taken forever) mutate their way around the molecular signal that Gleevec blocks, building drug resistance.

No wonder cancer is so much more vexing than heart disease. “You don’t get multiple swings,” says Bob Cohen, senior director for commercial diagnostics at Genentech. Use a drug that does not destroy the tumor completely and “the heterogeneity will evolve from the [surviving] cells and say, ‘I don’t give a rat’s ass! You can’t screw me up with this stuff.’ Suddenly you’re squaring and cubing the complexity. That’s where we are.” And that’s why the only chance is to attack the disease earlier—and on multiple fronts.

Three drugs, four drugs, five drugs in combination. Cocktails of experimental compounds, of course, were what doctors used to control HIV, whose rapidly mutating virus was once thought to be a death sentence. Virtually every clinician and scientist interviewed for this story believes a similar approach is needed with the new generation of anticancer drugs. But once again, institutional forces within the cancer world make it nearly impossible.

Combining unapproved drugs in clinical trials brings up a slew of legal and regulatory issues that cause pharma companies to squirm. While many drug-company oncologists are as committed to the public’s well-being as government or cancer-center researchers, they have less flexibility to take chances on an idea. Ultimately, they need FDA approval for their investigational compounds. If two or three unapproved drugs are tested in concert, it’s even harder to figure out what’s working and what isn’t, and whether one drug is responsible for side effects or the combination. “It becomes much more challenging in the context of managing the databases, interpreting the results, and owning the data,” adds Lilly’s Pearce.

“If you look at the millions of mice that have been cured of cancer, and compare it to humans, you realize there just has to be something wrong with those models.”

Over dinner at Ouisie’s Table in Houston, M.D. Anderson’s Len Zwelling, who oversees regulatory compliance for the center’s 800-plus clinical trials, and his wife, Genie Kleinerman, who is chief of pediatrics there, have no trouble venting about the legal barriers that seem to be growing out of control. It takes no more than ten minutes for Kleinerman to rattle off three stories about trying to bring together different drug companies in clinical trials for kids with cancer. In the first attempt, the trial took so long that the biotech startup with the promising agent went out of business. In the second the lawyers haggled over liability concerns until both companies pulled out. The third, however, was the worst. There were two drugs that together seemed to jolt the immune system into doing a better job of targeting malignant cells of osteosarcoma, a bone cancer that occurs in children. “Working with the lawyers, it was just impossible,” she says, “because each side wanted to own the rights to the combination!”

CHANGING THE WAY WE THINK ABOUT CANCER

STRANGE AS IT MAY SEEM, much of our failure in fighting cancer— and more important, much of the potential for finally winning this fight—has to do with a definition. Some 2,400 years ago the Greek physician Hippocrates described cancer as a disease that spread out and grabbed on to another part of the body like “the arms of a crab,” as he elegantly put it. Similarly, medical textbooks today say cancer begins when the cells of an expanding tumor push through the thin protein “basement” membrane that separates them from another tissue. It’s a fancy way of saying that to be cancer, a malignant cell has to invade another part of the body.

Michael Sporn, a professor of pharmacology and medicine at DartmouthMedicalSchool, has two words for this: “Absolute nonsense!” He goes on: “We’ve been stuck with this definition of what cancer is from 1890. It’s what I was taught in medical school: ‘It’s not cancer until there’s invasion.’ That’s like saying the barn isn’t on fire until there are bright red flames coming out of the roof.”

In fact, cancer begins much earlier than that. And therein lies the best strategy to contain it, believes Sporn, who was recently named an Eminent Scholar by the NCI: Let’s aggressively find those embers that have been smoldering in many of us for years—and douse them before they become a full-fledged blaze. Prevent cancer from ever entering that deadly stage of malignancy in the first place.

Sporn, who spent more than three decades at the NCI, has been struggling for many years to get fellow researchers to start thinking about cancer not as a state of being (that is, an invasive group of fast-growing cells) but as a process, called carcinogenesis. Cancer, as Sporn tells it, is a multistage disease that goes through various cell transformations and sometimes long periods of latency in its progression.

Thus, the trick is to intervene earlier in that process—especially at key points when lesions occur (known to doctors as dysplasias, hyperplasias, and other precancerous cell phases). To do that, the medical community has to break away from the notion that people in an early stage of carcinogenesis are “healthy” and therefore shouldn’t be treated. People are not healthy if they’re on a path toward cancer.

If this seems radical and far-fetched, consider: We’ve prevented millions of heart attacks and strokes by using the very same strategy. Sporn likes to point out that heart disease doesn’t start with the heart attack; it starts way earlier with the elevated blood cholesterol and lipids that cause arterial plaque[1]. So we treat those. Stroke doesn’t start with the blood clot in the brain. It starts with hypertension. So we treat it with both lifestyle changes and drugs. “Cardiovascular disease, of course, is nowhere near as complex as cancer is,” he says, “but the principle is the same.” Adds Sporn: “All these people who are obsessed with cures, cures, cures, and the miraculous cure which is still eluding us, they’re being—I hate to use this word, but if you want to look at it pragmatically—they’re being selfish by ignoring what could be done in terms of prevention.”

The amazing thing about this theory—other than how obvious it is—is that we can start applying it right now. Precancerous cell changes mark the progression to many types of solid-tumor cancers; many such changes are relatively easy to find and remove, and others are potentially reversible with current drugs and other treatments.

A perfect example is the Pap smear, which detects premalignant changes in the cells of the cervix. That simple procedure, followed by the surgical removal of any lesions, has dropped the incidence and death rates from cervical cancer by 78% and 79%, respectively, since the practice began in the 1950s. In countries where Pap smears aren’t done, cervical cancer is a leading killer of women.

Same goes for colon cancer. Not every adenomatous polyp in the colon (a lesion in the organ’s lining) goes on to become malignant and invasive. But colon cancers have to go through this abnormal step on their way to becoming deadly. The list of other dysplasia-like conditions goes on and on, from Barrett’s esophagus (a precursor to cancer there) to hyperkeratosis (head and neck cancers). Obviously, doctors are already doing this kind of testing with some cancers, but they need to do it much, much more.

Some complain that the telltale biomarkers of carcinogenesis, while getting more predictive, still are far from definitive, and that we should wait until we know more. (Sound familiar?) Researchers in heart disease, meanwhile, have taken an opposite tack and been far more successful. Neither high cholesterol nor hypertension guarantees future cardiovascular disease, but they’re treated anyway.

A few cancer researchers have made great strides in finding more early warning signs—looking for protein “signatures” in blood, urine, or even skin swabs that can identify precancerous conditions and very early cancers that are likely to progress. For instance, Lance Liotta, chief of pathology at the NCI, has demonstrated that ovarian cancer can be detected by a high-tech blood test—one that identifies a unique “cluster pattern” of some 70 different proteins in a woman’s blood. “We’ve discovered a previously unknown ocean of markers,” he says. And it’s potentially a mammoth lifesaver. With current drugs, early-stage ovarian cancer is more than 90% curable; late stage is 75% deadly. Early results on a protein test for pancreatic cancer are promising as well, says Liotta.

Yes, the strategy has costs. Some say wholesale testing of biomarkers and early lesions—many of which won’t go on to become invasive cancers—would result in a huge burden for the healthcare system and lead to a wave of potentially dangerous surgeries to remove things that might never become lethal anyway. But surely the costs of not acting are much greater.

Indeed, it is an encouraging sign that Andy von Eschenbach, director of the NCI, and Elias Zerhouni, who leads the NIH, are both believers in this strategy. “What our investment in biomedical research has led us to is understanding cancer as a disease process and the various steps and stages along that pathway—from being very susceptible to it, to the point where you get it, and ultimately suffer and die from it,” says von Eschenbach, a former urologist who has survived prostate and a pair of skin cancers. So, he says, he wants to lead the NCI on a “mission to prevent the process from occurring in the first place or detect the occurrence of cancer early enough to eliminate it with less morbidity.”

HOW TO WIN THE WAR

THERE HAS BEEN TALK like this before. But the money to fund the assault never came. And several cancer experts interviewed for this story worry that the new rhetoric from the NCI, while encouraging, has yet to move beyond lip service.

For the nation finally to turn the tide in this brutal war, the cancer community must embrace a coordinated assault on this disease. Doctors and scientists now have enough knowledge to do what Sydney Farber hoped they might do 33 years ago: to work as an army, not as individuals fighting on their own.

The NCI can begin this transformation right away by drastically changing the way it funds research. It can undo the culture created by the RO1s (the grants that launched a million me-too mouse experiments) by shifting the balance of financing to favor cooperative projects focused on the big picture. The cancer agency already has such funding in place, for endeavors called SPOREs (short for specialized programs of research excellence). These bring together researchers from different disciplines to solve aspects of the cancer puzzle. Even so, funding for individual study awards accounts for a full quarter of the agency’s budget and is more than 12 times the money spent on SPORE grants. The agency needs to stop being an automatic teller machine for basic science and instead use the taxpayers’ money to marshall a broad assault on this elusive killer— from figuring out how to stop metastasis in its tracks to coming up with testing models that better mimic human response.

At the same time, the NCI should commit itself to finding biomarkers that are predictive of cancer development and that, with a simple blood or urine test (like PSA) or an improved molecular imaging technique (PET and CT scans), can give patients a chance to preempt or control the disease. For that matter, as a nation we could prevent tens of thousands of cancers—and 30% of all cancer deaths, according to the NCI—by getting people to stop smoking. This all-too- obvious observation was made by every researcher I interviewed.

Alas, this is not a million-dollar commitment. It’s a billion-dollar one. But the nation is already investing billions in research, and that doesn’t even include the $64 billion a year we spend on treatment. To make the resource shift easier, Congress should move the entire federal war chest for cancer into one bureaucracy, not five. Cancer research should be managed by the NCI, not the VA and Pentagon.

Just as important, the cancer leadership, the FDA, and lawmakers need to transform drug testing and approval into a process that delivers information on what’s working and what’s not to the patients far faster. If the best hope to treat most cancer lies in using combinations of drugs, we’re going to have to remove legal constraints and give drug companies incentives to test investigational compounds together in shorter trials. Those should be funded by the NCI—in a process that’s distinct from individual drug approval. One bonus for the companies: If joint activity showed marked improvement in survival, the FDA process could be jump-started.

“It’s going to require a community conversation to facilitate this change,” says Eli Lilly’s Homer Pearce. “I think everyone believes that at the end of the day, cancer is going to be treated with multiple targeted agents—maybe in combination with traditional chemotherapy drugs, maybe not. Because that’s where the biology is leading us, it’s a future that we have to embrace—though it will definitely require different models of cooperation.”

MIRACLE CURES THAT WEREN’T

Decades of breakthroughs have raised hopes again and again for people with cancer—but have failed to deliver on expectations.

Radiation therapy Soon after Wilhelm Roentgen’s discovery of X-rays in 1895, some doctors predicted that the high-energy waves from exotic “cyclotrons” could be used to kill most cancerous tumors. A century-plus later, targeted radiation is a critical weapon in the oncologist’s arsenal but not the magic bullet many thought.

Interferon In 1980, the world was afrenzy about the big “IF”—an immune-system booster produced by the body in tiny quantities—as word spread that this natural virus fighter could also shrink tumors. Though still in use in some cancer therapies, IF has not fulfilled its early promise.

Interleukin-2 Like Interferon, this protein helps activate the body’s immune system. And like IF, IL-2 was once thought to be the “cancer breakthrough” we were waiting for (see FORTUNE’s 1985 cover, lower right). But after years of testing and tweaking, the therapy has led to only scattered remissions in patients.

Endostatin After a flurry of early hype, this first of many compounds designed to fight tumor angiogenesis failed dramatically in human tests. The jury is still out on its next-generation kin.

Gleevec The little yellow pill from Novartis has wondrous effect in a few rare cancers involving simple mutations, although the disease can grow resistant to this “targeted” biological drug.

When clinical trials begin to offer patients more than incremental improvements over existing drug treatments, people with cancer will rush into the studies. And when participation rates go up, it will accelerate the process so that we can test more combinations faster and cheaper.

To see which drugs truly have promise, however, we need to do one thing more: test them on people in less advanced stages of disease. The reason, once again, comes back to cancer’s genetic instability— a progression that not only ravages the body but also riddles tumors with mutations. When cancer patients are in the end stage of the disease, drugs that might have a potent effect on newer cancers fail to show much progress at all. Our current crop of rules, however, pushes drug companies into this can’t-win situation, where the only way out is incremental improvements to existing therapies. Drugs that might well help some cancer patients are now getting tossed by the wayside because they don’t help people whom they couldn’t have helped in any case. This has to stop.

Witness what has happened with the new class of drugs developed to fight the process called angiogenesis (“angio” refers to blood vessels, and “genesis” to new growth)— compounds designed to block the development of capillaries that supply oxygen and nutrients to tumors. Avastin is the best known, but there are some 40 anti-angiogenesis drugs in clinical trials.

This, by the way, is one of those big ideas that the cancer culture didn’t take seriously, and would barely fund, for decades. The concept was pioneered 43 years ago by Judah Folkman, now a surgeon at Children’s Hospital Boston. While studying artificial blood in a Navy lab, he was struck by a simple and seemingly obvious idea: Every cell needs oxygen to grow, including cancer cells. Since oxygen in the body comes from blood, fast-growing tumors couldn’t develop without access to blood vessels.

Folkman later figured out that tumors actually recruited new blood vessels by sending out a protein signal. If you could turn off that growth signal, he reasoned, you could starve the tumors and keep them tiny. The surgeon submitted a paper on his experiments to various medical journals, but the article was rejected time and again. That is, until an editor at the New England Journal of Medicine heard Folkman give a lecture and offered to publish it in the Journal’s Beth Israel Hospital Seminars in 1971—ironically, the year the War on Cancer began.

“It’s like a Greek tragedy,” says Intel’s Andy Grove. “Everybody plays his part, everybody does what’s right by his own life, and the total just doesn’t work.”

After decades of resistance, the cancer culture has finally come around to Folkman’s thinking—as the reception greeting Avastin makes clear. Still, the biggest promise of anti-angiogenesis drugs will be realized only when doctors can use them to treat earlier-stage patients. That’s because the drugs designed to choke the tumor’s blood supply often take a far longer time to work than traditional toxic chemo—time that people with advanced disease and fast-growing cancers may not have. Doctors also need the freedom to administer such drugs in combination. Tumors recruit blood vessels through several signaling mechanisms, researchers believe, so the best approach is to apply several drugs, cutting off all routes.

Who knows? A new paradigm in treatment may emerge from Folkman’s 40-year-old idea. Yet to make this simple and seemingly obvious shift, the entire cancer culture must change—from the rules governing drug approval to tort law and intellectual property rights. Science now has the knowledge and the tools; we need to act.

THE GOOD DOCTOR

IN THE WEEKS SINCE I finished my reporting and began writing this story, one image has stuck with me: a drawerful of letters. The letters belong to Eric Winer, a 47-year-old physician at Dana-Farber. He and I had been talking for close to an hour when he showed me the drawer.

It was late on a Friday evening, and Winer, still in the clinic, was describing the progress we were making in this war, his reedy voice cracking higher every so often. He was telling me of his optimism. That’s when he mentioned the drawer: “That enthusiasm is very much tempered by the fact that we have 40,000 women dying of breast cancer every year. Um, and you know, I’ve got a file full of letters that are almost entirely from family members of my patients who died….”

I asked to see it, and then asked again, and there it was, in the bottom drawer of his filing cabinet—two overstuffed folders of mostly handwritten notes. Once the letters go in, Winer confessed, he never looks at them again. “I don’t go back,” he said sheepishly. “My excuse initially was that if anyone wanted to say I was a bad doctor, I’d hold on to these things that people said about me. And I could prove that I wasn’t.”

If the walls of his office are any indication, there is no way Winer is a bad doctor. They are covered with loving mementos from patients. There is a picture of Tolstoy from a woman whose breast tumors were initially shrunk by Herceptin, but who died within five years. (Winer had once mentioned to her to that he had majored in Russian history at Yale.) There’s a photo of the Grand Canyon taken by a young nurse who was determined to take a trip out West with her 10-year-old son before she died. The daughter of another patient even cornered Lance Armstrong and begged him to sign a neon-yellow jersey for Winer, who is an avid cyclist. It is the most prominent thing in his office.

No, it isn’t just the patients in this War on Cancer who need renewed hope. It is the foot soldiers as well.

ADDITIONAL REPORTING Doris Burke FEEDBACK cleaf at fortunemail.com

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Footnotes

1 Numerous articles have been denouncing the cholesterol-heart-disease story as a myth. More ammunition has come from a recent large-scale study showing that high cholesterol levels seem to be associated with lowered cancer risk, see On the link between cholesterol and cancer incidence.

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