Cancer’s Many Faces of Resistance

Jocelyn Kaiser
Science Now

The big push in cancer treatment these days is to sample a person’s tumor, test it for mutations, and give the patient a drug tailored to a genetic weak spot in the tumor. A new study suggests one reason why this targeted drug strategy doesn’t always work. A solid tumor, it turns out, is not a mass of identical cancerous cells but a mosaic of genetically different cells that aren’t captured with a single biopsy. Some of these distinct cells may be resistant to the targeted drugs, allowing a tumor to persist or grow.

The classic view of how cancer develops is that a single, normal cell accumulates mutations that eventually allow or force it to divide uncontrollably. This “clone” then grows into a tumor of identical cells, which can also sow seed cells into the bloodstream that then take root somewhere else in the body, or metastasize. The assumption that tumors grow out from a single clone has spurred a rush to find drugs that block one of the clone’s genetic weak spots. But although the strategy has resulted in some very effective drugs—Iressa for lung cancer and a new melanoma drug called Zelboraf, for example—these drugs often stop working within a year or two. One reason could be that solid tumors already harbor a few cells, or clones, with “resistance” mutations that take over when the cells targeted by the drug are wiped out.

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