(2 of 3)
Since 60% to 70% of breast cancers grow in response to estrogen, half a dozen drugs, beginning with tamoxifen, introduced in the late '70s, work by blocking that hormone. Such drugs prevent cancer recurrences for 10 years or more in 50% of women with estrogen-sensitive tumors. Even for those with metastatic disease, hormone therapy can lengthen life and frequently will be more effective than chemotherapy. (Edwards told TIME, however, that her cancer was only slightly sensitive to estrogen, though she's waiting for new biopsy results to reveal "what receptors and markers I have.")
Many newer drugs target other pathways for tumor growth. Herceptin, introduced in 1998, interferes with a protein called epidermal growth factor by blocking the her2 receptor, a binding site that is found on the surface of many cells but is overabundant in about 25% of breast cancers. Other smart drugs interfere with the same growth factor, using slightly different chemical strategies to do so, and some have proved useful in a range of cancers. Gleevec, for example, which was approved in 2001, prevents growth factors from attaching to cancer cells and activating an enzyme called tyrosine kinase, which regulates cell division.
Gleevec reversed the odds for patients suffering from two rare cancers chronic myelogenous leukemia and gastrointestinal stromal tumors for which there had been no effective treatments. In a matter of months, patients who were out of options had their lives back, and while their cancer was not cured, it was under control, at least for a while. Other new drugs, including Tarceva and Iressa, also halt tumor growth by messing with tyrosine kinase. The key to developing such drugs, says Glaspy, is "torturing cancer cells, and getting them to confess to us which pathways they are dependent on."
Researchers have wrung other kinds of information out of cancer cells, including the way they spur the formation of blood vessels, which nourish their growth. Avastin, approved in 2004, is the first drug to throw a wrench into the process by suppressing a tumor's ability to recruit vascular growth factors. As with many of the newer therapies, doctors have found that it works best as part of a cocktail of cancer drugs.
Newer additions to this growing arsenal are being developed at such a clip that "it's fun to be an oncologist right now," says Hayes, though he's worried about sharp cuts in federal research spending. Hayes remembers wincing a bit 25 years ago when patients wistfully hoped that "something new will come along" to save them. "Now there's something new coming down the pike all the time," he says. In fact, an alternative to Herceptin was approved this month, giving doctors something to try when Herceptin stops working.