Cancer-fighting cell receptor cloned.

Cancer-fighting cell receptor cloned

Researchers have deciphered the genetic code for a receptor molecule that serves as the docking site for a naturally occurring cancer-fighting compound. The achievement may help explain why treatment with the compound, called tumor necrosis factor (TNF), has yielded inconsistent results in cancer patients, and may lead to improved cancer therapies, the researchers say.

Produced in small quantities by white blood cells, TNF can directly attack tumor cells and can activate other immune-system cells to attack cancerous tissues. But when physicians give high doses to cancer patients, TNF sometimes helps, sometimes has no effect, and sometimes induces severe side effects.

The key differences between TNF's good and bad sides may become clear with a better understanding of the compound's receptor, says Gale Granger of the University of California, Irvine, who led the effort to clone the TNF receptor.

While TNF receptors normally reside on the membrances of white blood cells, some cancer patients have circulating versions of the receptor in their blood. Grange suggests that these soluble receptors may "mop up" therapeutic doeses of the drug before it gets to its tumorous target. Knowledge gained from cloning the receptor may someday enable physicians to "get rid of the circulating receptors first, give the TNF [to a cancer patient], then add more receptors" to sop up any excess that could cause side effects, he says. Moreover, further analysis of the receptor's structure may reveal details about how it functions, providing an opportunity to modify its activity, the researchers assert in the April 20 CELL.