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  • That's because a tumor is made up of a hodgepodge of cells containing different genetic mutations, each of which allows it to wreak a different brand of havoc. Some mutations spur rapid growth; others prod nearby blood vessels into sprouting new capillaries; still others send cancer cells out into the bloodstream, where they can seed new tumors. Within 10 years, predicts Robert Weinberg, a cancer biologist at the Whitehead Institute in Cambridge, Mass., "we will analyze the mutant genes and then tailor-make a treatment [for] that particular tumor."

    One day there will be drugs to trip up a cell at each of the steps it takes on the path to malignancy. A patient with lung cancer, say, might undergo gene therapy, breathing in genetically altered cold viruses that don't cause infection but instead act as miniature delivery vans carrying copies of the p53 gene. Good copies of this gene, which is mutated in many cancers, can force some cancer cells to commit suicide. The effects of p53 could be bolstered with antibodies that slow tumors by attaching to the surface of cancer cells and gumming up their ability to take over the body's growth factors, the specialized proteins that promote cell reproduction.

    If a tumor has acquired the mutations for spreading, the doctor of the future may call on matrix metaloproteinase inhibitors, a new kind of drug that can be taken orally to block the enzymes a tumor uses to break down the cells of surrounding tissue and invade it. Vaccines cobbled together from whole cancer cells or bits and pieces of those cells have been shown to boost the body's immune system, helping it recognize and kill tumors on its own. "This was all a dream five years ago," marvels John Minna, director of the Hamon Center for Therapeutic Oncology Research at the University of Texas Southwestern Medical Center in Dallas.

    Also close to reality are the so-called antiangiogenic factors, relatively nontoxic compounds that inhibit the growth of new capillaries. The idea behind this new class of drugs is that tumors cannot grow bigger than a few hundred thousand cells--about the size of a peppercorn--without growing their own blood-supply system. Researchers and patients, not to mention the owners of stock in half a dozen biotech companies, are eagerly awaiting results of clinical trials of antiangiogenic factors, which might be used in combination with chemotherapy to knock down big tumors and then prevent any surviving tumors from growing enough to do further damage.

    The assumption behind many of these futuristic scenarios is an idea that most researchers have begun to embrace but that many patients will undoubtedly find difficult to accept. That is the prediction that certain cancers may require treatment for the rest of a patient's long life. Coming out of a century that declared war on the disease, a century that felt the only reasonable response to a tumor was to annihilate it, this may be hard to imagine. But turning cancer into a controllable condition is not so different from treating high blood pressure or diabetes. "I don't think curing cancer is the goal," says Ellen Stovall, executive director of the National Coalition for Cancer Survivorship. Instead, she says, "it should be helping people live as long and as well as they can."

    No, we probably won't cure all forms of cancer in the 21st century. But we may very well learn to live with them.

    Science writer Shannon Brownlee's work has appeared in the New York Times, the New Republic and the Atlantic Monthly

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