The hoary metaphor of the war on cancer, as overused as it may be, is as evocative as ever to describe our efforts to beat the disease that will claim nearly 566,000 American lives this year alone. So let's fall back on martial imagery to describe our current position: We now know the enemy far better than ever before. And that promises much more precise targets.
Of course, as even Sun Tzu recognized, intel must be translated into effective action, and in this struggle, that effort has been all too plagued by failure. But mounting discoveries about the astoundingly complex essence of cancer—that its causes lie in multitudes of genes gone awry—are also pointing the way toward treatments aimed in laserlike fashion at a patient's unique set of genetic glitches. In mid-October, scientists reported in Nature that they've identified 26 key mutated genes linked to lung cancer, for example. "All of the pieces of the puzzle are in front of us," says Martin McMahon, a cancer biologist at the University of California-San Francisco Helen Diller Family Comprehensive Cancer Center. "It used to be that 10 percent of the pieces were in front of us and the other 90 percent were in a box under the stairs."
It's been clear for years, for example, that cancers vary widely even if they look the same under a microscope: Some are slow growing, others are aggressive; some patients respond to one drug, while others are not helped at all. Yet until quite recently, the only tools available—the blunt-force mainstays of surgery, chemotherapy, and radiation—treated everyone much the same. Then, in the 1990s, powerful new computing technology allowed researchers to begin comparing the DNA of cancerous and healthy tissues and gain a look at the very blueprints of similar-looking but markedly different tumors. Here's where the advances are leading:
Toward Personalized Treatment
Louise Cooper, an elementary school teacher and endurance athlete, is one early beneficiary. Now 55, she was diagnosed in 1998 with breast cancer and received the same basic knock-it-out treatment—surgery, chemo, radiation—prescribed for other women with similar-looking tumors. That's where Cooper's story diverged from the usual path: Her former neighbor is breast cancer expert Dennis Slamon, director of clinical and translational research at the University of California-Los Angeles Jonsson Comprehensive Cancer Center. Slamon and colleagues had discovered that in about a quarter of breast cancer patients, whose tumors were particularly aggressive, too many copies of a gene called HER2 within a cancer cell causes the overproduction of a certain protein on the cell surface that serves as a receptor for a growth-spurring substance. Cooper was tested at Slamon's suggestion and learned her tumor fit this description. "I found out that from diagnosis to demise, it's usually about two to three years, maximum," says Cooper, an L.A. transplant who grew up in South Africa.
But Slamon and his team had developed a drug that blocks the receptors, preventing the cell from getting the fix it needs to grow. After receiving weekly infusions of Herceptin for a year, Cooper is apparently cancer free—and off to Antarctica for a multiday 250-kilometer footrace just before Thanksgiving.
You might ask why Herceptin, now a weapon of choice in women whose tumors produce too much HER2, can't be used to block all sorts of cancer from growing. As science is revealing, there are thousands and thousands of mutated genes that contribute to cancer's uncontrolled growth and self-replication, refusal to die off, and ability to travel elsewhere in the body, lodge there, and thrive. As with HER2, a glitch might be found in some cancers in a particular organ but not others—and it may also be active in cancers in completely different organs. (HER2 is also associated with ovarian cancer.) In September, two research teams—one working on the government's massive new cancer gene-mapping initiative, the Cancer Genome Atlas project, and one on a separate private effort—described all the hundreds of possible mutations linked just to pancreatic cancer and a deadly form of brain cancer. The average pancreatic tumor, for example, included 63 mutations.