ices necks, then removed the tumors two weeks later, using the methods a surgeon would use to remove a tumor from a human. Half the mice then received daily p22 injections; half received a placebo. Two weeks later, the scientists weighed the mices lungs. The placebo groups lungs weighed more than three times as much as the p22 groups. The extra weight was due to cancerous growths, they said.

The researchers showed that p22 is a natural compound released by cancerous cells themselves to control blood vessel growth. Cancer cells must force new blood vessels to grow so they can obtain the nutrients necessary to continue rapidly dividing. Without a direct blood supply, a colony of cancerous cells cannot develop into a deadly tumor.

The p22 protein kills the cells that line the walls of growing blood vessels, thereby preventing new vessels from developing. Waisman hypothesizes that p22 is part of a sensitive growth control system. If a tumor releases compounds to both promote and inhibit endothelial cell growth, it has much more control over blood vessel growth than if it released only growth factors alone, he explained.

Waisman believes that p22s small size means scientists will be able to determine its molecular structure. With a small molecule, we can see it, see where it goes. Does it bind to a receptor? How can it specifically attack only capillary endothelial cells and no others? The real excitement is that were getting really close to figuring out how this works, said Waisman.

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Contact: Sharon Worthy
s_worthy@acs.org
202-872-4371
American Chemical Society
14-Nov-2001

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