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Blocking VEGF can enhance radiation therapy

Blocking the action of vascular endothelial cell growth factor (VEGF), a substance that encourages the growth of new blood vessels, can dramatically increase the anti-tumor effects of radiation therapy report medical researchers from the University of Chicago and Harvard medical schools in the July 15th issue of Cancer Research.

This report adds to the mounting enthusiasm for combining drugs that prevent the growth of new vessels -- such as angiostatin, endostatin and now anti-VEGF -- with other forms of cancer therapy.

"Despite all the media attention devoted to angiostatin and similar agents, most scientists suspect it's unlikely that, by themselves, these new drugs will have a very dramatic effect on most types of cancer," said Ralph Weichselbaum, M.D., professor and chairman of radiation oncology at the University of Chicago and director of the study.

"But we have long been certain," he added, "that radiation therapy works quite well for eradicating relatively small human tumors. Now we have good reasons to believe that combining radiation with angiogenesis inhibitors can make this well established treatment significantly more effective, perhaps even against comparatively large tumors, with very little added toxicity."

Angiostatin and endostatin provide a big boost to radiation therapy, Weichselbaum's group has shown in studies done with mice, but neither drug has begun the first phase of human testing. In this Cancer Research paper Weichselbaum and colleagues demonstrate that anti-VEGF, which is already in phase-II clinical trials, can have an equally dramatic impact.

The researchers' interest in vascular endothelial cell growth factor was piqued by their discovery that tumors produce three-to-six times more VEGF after exposure to radiation, and these elevated levels persist for up to two weeks. By speeding the growth of new blood vessels to supply the radiation-
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Contact: John Easton
jeaston@mcis.bsd.uchicago.edu
773-702-6241
University of Chicago Medical Center
15-Jul-1999


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