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The Death of Cancer
After Fifty Years on the Front Lines of Medicine, a Pioneering Oncologist Reveals Why the War on Cancer is Winnable â" and How We Can Get There
By Vincent T. DeVita Jr., Elizabeth DeVita-Raeburn Farrar, Straus and Giroux
Copyright © 2015 Vincent T. DeVita Jr., M.D., and Elizabeth DeVita-Raeburn
All rights reserved.
ISBN: 978-0-374-71417-8
CHAPTER 1
OUTRAGEOUS FORTUNE
In the third act of Hamlet, as the prince contemplates his own death, he refers to the "slings and arrows of outrageous fortune." It's a lovely turn of phrase for profound bad luck — bad luck of Shakespearean proportions. The kind of bad luck that leaves the recipient blindsided by the way life has changed on a dime.
I chose part of this phrase as the title of this chapter because it struck me that cancer is bad luck. Simply put, it's the bad luck to possess cells that have acquired the ability to refire the dormant machinery capable of driving rapid-fire fetal growth and to have lost the ability to stop it. It is bad luck on the order of Shakespeare because, as anyone who has ever been diagnosed (or loved someone who has) knows, the impact of cancer on one's body, one's life, and one's family is nothing short of epic.
And yet this outrageous turn of fortune happens, each year, to more than a million people in the United States, more now than in the past because our population has grown and because it is older. One day you are fine. The next, there you are, with Hamlet, feeling cornered and contemplating mortality, while others go about their ordinary lives.
The writer and critic Susan Sontag, who was herself diagnosed with leukemia, once said, "Illness is the night-side of life, a more onerous citizenship. Everyone who is born holds dual citizenship, in the kingdom of the well and in the kingdom of the sick. Although we all prefer to use only the good passport, sooner or later each of us is obliged, at least for a spell, to identify ourselves as citizens of that other place."
No one embarks upon this journey willingly. It is outrageous fortune that propels us there. The story I want to tell you is about how this journey has changed — how far we have come, and how far we have to go.
The most effective way to convey this is by telling you the story of a patient. In the spring of 1996, I was standing on my back deck grilling a piece of swordfish when I heard the sliding glass door open. I looked up and saw my wife, Mary Kay, walking toward me, the phone pressed to her chest. She had a look on her face that I have come to know well over the years: someone had cancer.
Calls like this one are not uncommon. Because my career has given me a certain degree of visibility and because I have a reputation as someone who believes in giving cancer patients every possible chance, people find me.
Mary Kay mouthed the name of the person on the phone: Lee, a family friend of twenty-five years. Mary Kay and Lee's wife, Barbara, had met in an art class in Washington and had remained close friends ever since, even after we'd moved to Connecticut. Lee and I had gradually become close friends over the years. He introduced me to stamp collecting, probably the least eccentric of his avocations, and I introduced him to opera, a passion that had consumed much of my free time for years.
With pin-straight white hair that constantly fell in his face, piercing blue eyes, and round, wire-rimmed glasses, Lee looked like a middle-aged Harry Potter. He was a reflexively cheerful guy, the kind of person who refused to see the downside of anything. Share a problem with him, and he'd pace your living room, or sit, legs crossed, foot waggling, while he drummed up a solution. Lee liked solving problems, and as an economist for the World Bank he'd solved problems all over Latin America and the Middle East.
I took the phone and handed Mary Kay the spatula. "Vince," Lee said, "sorry to bother you." The call wasn't a complete surprise. Lee and I had spoken earlier in the week, after a frightening morning in which he'd seen blood in his urine. Like most people, he'd immediately feared the worst. "It's probably nothing," I'd said. "But you should see your doctor."
His doctor assured him that, at sixty, Lee was probably too young to have cancer. He told him that a host of other conditions could produce blood in the urine. And when he examined Lee, he found none of the telltale lumps on his prostate gland that might have suggested cancer. His best guess, he told Lee, was prostatitis, an infection of the prostate gland. He gave Lee a prescription for an antibiotic. And just in case, he ordered a PSA test.
PSA, or prostate-specific antigen, is made by cells in the prostate gland. Cancer cells make more of it than do healthy cells, so an unusually high level of PSA can be an early indication of cancer. But, as many people know, the PSA is an imperfect test. Because it can raise more questions than it answers and can spark unnecessary anxiety, many doctors don't use it routinely. And many men opt not to get it, including me. But given the blood in Lee's urine, his doctor thought he should check Lee's level.
Lee's phone call was to tell me that his PSA result had come back. "The doctor said it was high," he said, sounding uncharacteristically shaky. I was concerned, too. Lee's results didn't sound good. I was torn between giving him the raw truth and shielding him a bit longer. I opted for the latter. I repeated what he'd already heard from his doctor. "You'll need to have a biopsy," I said. "That's the only way to make a diagnosis. We won't know anything for sure until then."
I told him to have his doctor send me the biopsy report when it was done. I didn't tell him that I thought he had cancer. But I was pretty sure he did. It's true that an elevated PSA doesn't always mean cancer. But the higher the score, the greater the likelihood that it does. A normal PSA is under four. Over ten suggests a strong probability of cancer. Lee's was twenty-three.
Lee had the biopsy that his doctor recommended. It came back positive. The next step was to get an MRI, a medical imaging technique well suited to scanning soft tissue. It revealed enlarged lymph nodes around Lee's prostate gland — not a good sign. The lymph nodes that surround organs are a gateway for cancer cells. If you find cancer cells there, odds are the cancer has already spilled out into blood vessels; it has metastasized.
Prostate cancer can be a tricky disease to treat. Many prostate cancers grow so slowly that the men who have them will die of old age before they die of the cancer. This is one of the things that makes the PSA test so controversial. When men are routinely given a PSA test as a screening tool, these cancers can turn up. As a consequence, men who might never have been bothered by their cancers end up undergoing extensive testing and treatment for something that would never have become life threatening. One study of samples taken from the cadavers of men over age fifty who had died of other causes found that approximately 31 percent had evidence of prostate cancer. Whatever killed those men had been more deadly than their prostate cancer. But if they'd been given PSA tests, they might well have been given unnecessary treatment for those slow-growing cancers.
We can't be totally complacent about the disease, however, because some prostate cancers are aggressive and quite deadly. Lee's was starting to look as if it was one of those. And there was another indication that it was a nasty tumor: the pathologist who looked at the tissue from Lee's biopsy gave it a high Gleason score. Devised by the pathologist Donald Gleason in the 1960s, this scoring system is a way to evaluate prostate cancer cells under a microscope and determine which are most aggressive. The higher the Gleason score, the worse the prognosis. A score lower than six usually means the cancer isn't too aggressive. In those cases, oncologists will often decide to withhold treatment and monitor the cancer to see whether it spreads — a practice called watchful waiting.
A Gleason score of seven to ten, on the other hand, suggests a patient will have a poor prognosis. The pathologist gave Lee's cancer a Gleason of ten, meaning the cells in his tumor appeared wild. They were large and had an unusual structure and more cytoplasm than a typical cell. More bad news. Cells with this appearance tend to behave autonomously — to have their own built-in signaling system. They are likely to grow out of control and invade other tissue. So far, all indications were that Lee's cancer was a very bad actor.
Aggressive, fast-growing cancers are difficult to track down and get rid of, but in the process of making copies of themselves, they have to disassemble their DNA for a brief time. At that moment, they are most vulnerable, and we can attack.
But we have to be smart about what we hit them with — and how aggressively. Cancer cells are cannily adaptive; they learn to outwit therapies quickly. So the first attempt to treat a cancer has the best odds of curing it, because we're hitting it with something it's never seen before. The cancer is more vulnerable and treatable than it will ever be again. This is one reason recurrences are so troubling: you're dealing with much smarter cells by then.
This was all going through my mind as Lee and I exchanged emails and phone calls during the week after his biopsy. Even with positive nodes and a high Gleason score, Lee had a chance — a slim one — that rested on getting that best first shot. We needed a doctor willing to try everything we had in our prostate cancer arsenal. That worried me more than Lee's soaring PSA.
When I was a young oncologist working the wards at the National Cancer Institute, we had the freedom to try anything and everything for each individual patient. We had fewer tools then, and you had to be flexible to maximize the chances for each patient. There was no prescription for how to handle a specific cancer because we were inventing it as we went along. Gradually, day by day and week by week, we figured out how to cure more people.
Over the years, we've gained more tools for treating cancer, but the old ability to be flexible and adapt has disappeared. Many doctors now rely on what are known as standards of care — treatment guidelines issued by professional organizations or government institutions. These are based on the advice of expert panels and evidence in published studies that spell out the best treatment for most patients with a particular kind of cancer. The standards of care also explain how and when the treatment should be used.
To establish these guidelines, doctors look at such things as typical responses to chemotherapy and the median survival curve — the length of time that 50 percent of patients will remain alive for a given treatment. The idea is to establish what's best for the largest number of patients. The guidelines have a big impact on care. The FDA uses them when considering drug approval, and insurance companies use them when deciding whether to reimburse patients for treatment. If a patient's treatment meets the standard of care, insurers will usually pay for it. If it deviates too far from that, insurers are likely to pronounce the treatment experimental or unproven and refuse to cover it.
Malpractice lawyers are ready to pounce on treatment that doesn't meet the standard of care, arguing that the patient they're representing didn't get the best possible treatment. As a result, doctors have strong incentives not to stray too far from the standard of care. And for many patients, this system does indeed help ensure that they will get the best treatment.
But this state of affairs also raises problems. Guidelines are backward looking. With cancer, things change too rapidly for doctors to be able to rely on yesterday's guidelines for long. These guidelines need to be updated frequently, and they rarely are, because this takes time and money. But if they're not revised to reflect advances in treatment, patients who might have been cured by newer approaches will die. Reliance on such standards inhibits doctors from trying something new.
My concern was about the standard-of-care guidelines for prostate cancer. Lee's situation wasn't well suited to the guidelines that were current in 1996. Neither surgery nor radiotherapy by itself could extend the median survival for those with prostate cancer that, in cases like Lee's, had already spread to the lymph nodes. According to the standard of care, therefore, doctors had dismissed these two forms of treatment in favor of what had worked best: administering drugs to block the naturally produced testosterone that stimulates the division of prostate cancer cells. Deprive those cells of testosterone, and you'll slow their incessant growth. For a time.
The problem was that although this approach improves median survival, it doesn't cure anyone, and everyone in the medical community knew it. All cancers are canny and adaptable. Prostate cancer cells eventually and inevitably found a way to grow, divide, and spread without the presence of testosterone. At best, this therapy, known as androgen deprivation therapy, or ADT, bought the patient a little time. As an oncologist, buying patients time is one of my primary strategies. Not so that they can get their affairs in order, or face the inevitable, but because I want to keep patients going until the next new treatment comes along so that they can take advantage of it. But Lee's cancer was so ferocious that I didn't think ADT would extend his life for more than two or three years — at best. I didn't think that was long enough to get us to the next advance. We needed more time.
I wasn't surprised when Lee called and told me that his urologist recommended that he go on ADT treatment. His urologist, I noted, hadn't told him the therapy would likely provide little benefit. That didn't surprise me either. It's not easy to deliver that kind of news, and many doctors simply don't do it. But I'm an aggressive doctor. I will do whatever it takes to cure patients and, if that isn't achievable, keep them going as long as possible. So the bigger issue, from my perspective, was whether there was something else, something better than hormone deprivation, we could try. But I couldn't make Lee's decisions for him, so I did what his urologist had not: I explained the situation and asked him what he wanted.
"Ten years," he said. I asked him what he was willing to do. "Anything," he said.
I had an idea. Clinical studies of new cancer treatments report their successes or failures in the aggregate: what percentage of patients survived for five years, say, or how many gained a few months. But a search through the details in these studies often yields clues about what might work even better for a certain minority of patients.
Not many people have the time or expertise to search for and find such clues. But I do. It's what we did in the pioneering days at the National Cancer Institute, when survival rates were low and we looked everywhere for ideas as to what to try for our patients. It's the kind of thing a determined oncologist can do on behalf of a patient now if he or she is unwilling to settle for a ho-hum standard of care.
I had heard about a prostate cancer study at the Mayo Clinic where researchers were exploring the use of radical prostatectomy — removing the prostate gland and the surrounding lymph nodes — in patients whose nodes had not yet been infiltrated by spreading cancer cells. The standard operation in these cases was to remove only the prostate gland and leave these nodes, the assumption being that removing the nodes as well made the surgery more extensive without affecting the odds. There wasn't any evidence that survival could be extended by removing nodes to which cancer cells had not apparently yet spread. Why bother?
The Mayo group had discovered, however, that in about a third of cases there was undetected spread of the cancer to the lymph nodes. Nodes that appeared to be free from cancer cells were not. And the Mayo researchers were finding that removing the nodes in these patients improved survival. The researchers hadn't seen enough of an impact to justify the treatment for all people with prostate cancer and lymph node involvement. But about 15 percent of treated patients were surviving free of disease.
I found this particular number — practically a footnote in the article — to be more interesting than the researchers suggested. It was a better result than what I'd seen in most other novel therapies at that time for metastatic prostate cancer, which is what Lee had. I thought it was worth a try for him. I called the chief surgeon of the group and asked if he would see Lee. Then I asked Lee whether he was willing to make the trek to Minnesota, where he might have major surgery away from most of his family. He agreed to give it a try. Unfortunately, when doctors at the Mayo Clinic examined him, they decided that his cancer was too advanced for their study. They refused to operate.
(Continues...)
Excerpted from The Death of Cancer by Vincent T. DeVita Jr., Elizabeth DeVita-Raeburn. Copyright © 2015 Vincent T. DeVita Jr., M.D., and Elizabeth DeVita-Raeburn. Excerpted by permission of Farrar, Straus and Giroux.
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