In recent years, some surgeons have learned a more dramatic way to map these vital areas. Many now perform brain surgery on
patients who are not knocked out by anesthesia (this is possible because the brain itself is not sensitive to pain). Senator
Ted Kennedy—who underwent surgery at Duke—was one such patient. In so-called “awake surgery,” the medical team can stay in
constant communication with the patient, asking him to recite a sentence or to grip a ball, in order to make sure they’re
not cutting into a part of the brain that would cause major damage. What this means is that surgeons can be much more aggressive;
they can cut out more of the tumor, without having to leave a large margin of error to protect sensitive brain regions. But
it’s still not a cure. We’re pretty much at a limit with what we can do surgically, because we can only take out what we can
see. And at this level, the real problem is the tumor cells that we can’t see.
Put it all together, and the diagnosis has been historically a death sentence. Without treatment, the average survival time
is just a few months. With standard treatment—surgery to cut out the tumor, followed by radiation and chemotherapy—most patients
still die in less than a year. Just 3 percent make it five years—and these are patients who are relatively young for cancer,
often in their thirties, forties and fifties.
16
A
WEEK AFTER SURGERY
, David Bailey went to meet with his doctor, expecting to strategize about how to save his life. “They took out the staples
and stitches. And then I said, ‘So what’s the plan?’ He suggested a guy I might want to call,” says Bailey. “I said, ‘Well,
do you have a number?’ And then, ‘Can I use your phone?’ I’d done some research, and I knew this thing doubled in size every
ten days. Here, it had already been twelve days.” Bailey could tell his doctors weren’t feeling the urgency, so he had to
ask, “Is this always lethal?”
“It’s pretty hard to beat” was the limp reply.
GBM is such a grim diagnosis that many doctors won’t even try to beat it. They’ll push patients straight toward end-of-life
care, treatments meant to ease suffering rather than fight the disease. But David Bailey wasn’t ready for that. To find hope
in a hopeless situation, Matt Pfenninger turned to prayer; Bailey turned to the Internet. He got home and started surfing
the web. With an old dial-up modem, it took a while, but he found a website,
www.virtualtrials.com
, that listed all the experiments, all the trials of potential new ways to beat this hopeless condition. He felt a little
better, but only until he started calling, with that white-knuckled grip on the phone.
“I called the first number, and said, ‘Hello, I’m Dave Bailey. I have a brain tumor. Can you help?’ ” remembers Bailey.
“What do you have?”
“Glioblastoma.”
“Ohhhhhh.”
Says Bailey, “You could hear it in her voice.” And in the voice of the next person he called, and the next. “I’d get that
same depressed tone of voice, basically saying, ‘There’s not much I can do.’ I’d just hang up. This was not what I was looking
for.”
And that’s how it went, all the long, long day: one dead end after the other. But then on the twenty-fourth call, he heard
something different. “This girl answered the phone, and I gave a little speech. She said, ‘Oh, yeah? Tell me all about it.’
Just this little change in tone. I said, ‘Yeah, I’ll tell you everything.’ She was empathetic, caring, and at the end she
said, ‘I’ll give the doctor all the details, and he’ll call you tonight.’ ”
Somehow, her good-bye was a letdown; after dozens of dead ends, Bailey figured he was being blown off, again. But at ten thirty
that night, the phone rang. “There was this voice, saying, ‘Hi, I’m Dr. Friedman at Duke. I hear you’ve got a brain tumor.
What are we going to do about it?’ And I said, ‘I don’t know, but you’re hired.’ ”
The voice on the line was Dr. Henry Friedman, the deputy director of the Preston Robert Tisch Brain Tumor Center. When I sat
down and spoke with Henry Friedman, he was dressed in a Duke sweatshirt and a pair of jeans. He wasn’t exactly what I expected.
With almost an irreverent sense of humor, he quickly charmed everyone in the room. What struck me the most was how often his
cell phone rang. I came to learn that he gives his number to all of his patients and strongly encourages them to call. It’s
all part of the healing that he offers.
Friedman says that what happened to Bailey is typical. “Almost every patient I see, a physician has said they’re dead before
they even get to us. Virtually everyone,” says Friedman. Too many doctors, he says, think there’s nothing to be done for patients
like Bailey. That means Friedman’s first battle is against perception. “You don’t have to die of GBM. It’s not a given, and
because it’s not a given, we can offer interventions that are more optimistic. Hope is the real card you play. It’s very critical
in any battle, against any illness.” That was the message David Bailey had been waiting to hear. The next morning, he and
his wife packed his brain scans into an envelope, packed up the car, and drove the four hours to Durham.
This was 1996, and after a new round of brain scans and meetings, Bailey was put on a drug called temozolomide, which today
is sold under the brand name Temodar. Bailey was just the twelfth person ever to get it. Friedman was as optimistic as he
could be under the circumstances. Bailey was an energetic young man, and his initial operation had cut the tumor down to the
size of a lentil. And for three months, the news was good. With temozolomide, along with standard chemotherapy and radiation,
Bailey’s brain scans were clear.
After radiation and drug therapy, standard treatment would have been to leave well enough alone. But Bailey and Friedman weren’t
done. During the second surgery, surgeon Allan Friedman (no relation to Henry) had inserted a port, or shunt, a tube physically
implanted in Bailey’s brain through which another experimental treatment could be administered.
The approach is called monoclonal antibody therapy. Proteins from a malignant glioma are loaded onto human immune cells, which
learn to react to those proteins. These cells are cloned in the lab and bonded to radioactive iodine. Administered through
the shunt, the treatment is supposed to work like a smart bomb. Guided by the immune cells, the radiation goes on a search
and destroy mission straight to the cancer cells, leaving the surrounding brain tissue unhurt.
For Bailey, the experience was a bit unsettling. Every day, an official from the Nuclear Regulatory Commission would come
to Bailey’s hospital room with a Geiger counter to make sure the radiation from the antibodies wasn’t seeping into the rest
of the hospital. But Bailey responded well—very well. In the vast majority of GBM cases, the cancer comes back within a few
months, and the patients die a few months later. But by the time my team met David Bailey, he had gone more than a dozen years
without a trace of malignant growth. That’s a spectacular result. So good, you
might
call it a miracle.
But it pays to dig deeper. Scientifically speaking, Bailey is an outlier. Diagnosed with an invariably deadly brain cancer,
he beat incredible odds. How? As I have said, most doctors don’t believe in divine intervention; they believe that if a patient
gets better, there must be a good reason. Now, we might have a tendency to give ourselves too much credit—to say that whatever
the physician did is the thing that cured the patient. But there is a plus side as well. It means we are always looking for
an underlying reason—a lesson to learn that might help others. It is fair to say that just because we find a scientific explanation
for something doesn’t make it less wonderful—less miraculous, if you will. The fact that we can detect religious feeling on
brain scans doesn’t make those feelings of awe any less powerful.
In any case, a survival story like Bailey’s is a great big puzzle. It’s a mystery where the clues are so tiny that they can
only be seen at the end of a powerful microscope, in chemical bonds, and the makeup of our human DNA. It’s instructive to
look at the clues one by one. Think of it as the scientific dissection of a miracle. Like others in these pages who have cheated
death, Bailey had a few things going for him. For one thing, he was young, and younger glioblastoma patients are known to
do better.
17
Before his cancer, he was generally healthy, and he was given a multitude of treatments, some conventional and some experimental.
He also got surgery, traditional chemotherapy, standard radiation, a new experimental drug, and then the experimental monoclonal
antibodies. Which treatment, or treatments, was critical to his survival?
We can’t say for sure. By now, many other patients at Duke and other academic cancer centers like UCLA and M. D. Anderson
Cancer Center in Houston have received the same experimental treatments as Bailey did, as well as a few newer therapies. There’s
been a measure of success—in some studies of monoclonal antibody treatment, average survival nearly doubled to almost two
years—but almost no one makes it a dozen years, certainly not without a hint of trouble.
18
So what is it about David Bailey? Is he just a statistical quirk? Does he have good luck? Did God choose to save his life?
Or is there something about his story that just might help other patients?
T
HE PRESTON ROBERT
Tisch Brain Tumor Center is a place where they try to put the puzzle together. Dr. Darrell Bigner, the director, is a soft-spoken
man with a courtly southern drawl. In a storied scientific career, he has laid the groundwork for a number of cutting-edge
treatments, including monoclonal antibodies, an approach that his lab first developed. Yet despite some advances against brain
cancer, Bigner says bluntly that the disease is winning the battle. “It’s still a poor prognosis. There have only been two
new treatments in the last thirty years, and to tell you the truth, neither of them is terribly effective,” says Bigner. “[On
average] they might extend life, and quality of life, by just a few months.”
According to the National Cancer Institute, the standard of care for glioblastoma is surgery, followed by radiation and Temodar.
19
That combination has been shown to increase average survival by about two months compared to radiation alone.
20
That’s not bad, but it isn’t great, either. We clearly need something better. That’s why Henry Friedman and the other doctors
at Duke put so much emphasis on clinical trials. About two-thirds of the brain cancer patients who come through the door at
Duke are put on an experimental protocol.
21
“Surgery, radiation, Temodar—we just don’t think that’s good enough. We don’t think that’s adequate,” says Friedman.
If insurers will pay—and Friedman is aggressive in pushing them—almost every patient gets something extra: an experimental
drug, procedure, or vaccine, for instance. The first extra tends to be Avastin, a monoclonal antibody that works to block
the growth of blood vessels that feed tumors. After years of promising results from this experimental use, in May of 2009
the Food and Drug Administration officially approved Avastin as a treatment for GBM. (It had previously been approved to treat
colon cancer). Other patients at Duke are funneled toward studies on monoclonal antibodies fused with radiation—the treatment
Bailey got—or to anticancer vaccines.
A Duke vaccine trial that’s received a lot of attention lately involves a substance called CDX-110. In the 1990s, a number
of cancer researchers—Darrell Bigner among them—noticed something unusual happening with the proteins on the cell surfaces
of glioblastomas, as well as on breast, ovarian, prostate, and colorectal cancers. The protein that made them take notice
is known as epidermal growth factor receptor, or EGFR. In healthy cells, it binds to another protein, epidermal growth factor
(EGF), part of a process that’s vital to the controlled division of cells.
The researchers noticed that there was a lot more EGFR on the surfaces of tumor cells than there was on the healthy cells.
What’s more, cancerous cells often display a mutation of EGFR, a version with a name right out of a
Star Trek
episode: EGFRvIII, or EGFR factor three. According to Dr. John Sampson, a cancer specialist at Duke, if EGFR is a switch
controlling cell division, EGFRvIII is a switch that’s “on” all the time—constantly signaling the tumor cells to divide.
22
Identifying this protein meant that cancer specialists had a target. Scientists from several major centers, including Duke,
Stanford, Johns Hopkins, and M. D. Anderson all played a big role. They took a portion of the EGFRvIII protein and combined
it with other substances that send the body’s immune system into overdrive. When injected, the vaccine triggers the body’s
immune system to attack any cell that’s loaded with the mutant version of EGFR—in other words, the tumor cells. It’s like
a heat-seeking missile. In an initial study where patients got CDX-110 along with Temodar and radiation, the vaccine more
than doubled survival time. The average patient lived more than two years, instead of just a year.
23
At Duke, the difference is palpable. Patients used to go home for a few months and die—now they come in with complaints like
broken bones from skiing accidents. Says Sampson, “We see people back now that are having complaints and problems that you
just don’t
see
in people with brain tumors. Like a guy four years out [from his diagnosis], who should have been dead three years ago—he’s
out skiing, and hurt his knee.”
Imagine hearing stories like this when you’ve just been given six months to live. They mean hope. Sampson says, “You can’t
give people hope, unless you can show people someone who’s done well. It’s like jumping out an airplane without a parachute.
You can be as optimistic as you want on the way down—it doesn’t change the outcome. But it’s different if you can point to
a second rip cord.”