New Targets Found That Stop Tumor Growth

Blocking blood vessel formation has already worked against breast, colon cancers

FRIDAY, May 2, 2008 (HealthDay News) -- A number of potential new targets for treatments that block tumor blood vessel formation -- a key step in tumor growth and metastasis -- have been identified by researchers at the University of North Carolina at Chapel Hill.

The use of the drug bevacizumab (Avastin) to target the formation of blood vessels (angiogenesis) that feed tumors has proven successful in treating breast and colon cancer, according to background information in the study. The drug inhibits a protein called vascular endothelial growth factor (VEGF), which plays a major role in angiogenesis.

"There is a large amount of data that shows if you block angiogenesis, you can block tumor growth. But VEGF is not responsible for all of angiogenesis. We wanted to identify more targets for this therapeutic approach," study senior author Dr. Nancy Klauber-DeMore, an associate professor of surgery in the UNC School of Medicine, said in a prepared statement.

She and her colleagues identified new targets after analyzing blood vessel cells in cancerous and normal breast tissue samples. They identified 1,176 genes that differed in activity or expression between the two cell populations. Of those, 55 genes were overexpressed more than fourfold in blood vessels from breast cancer.

"The most exciting aspect of this study is that we now have a very large list of potential targets that we will continue to work on for at least the next decade," Klauber-DeMore said.

So far, she and her colleagues have only looked at seven out of the 55 potential targets.

"This work points us in the direction we need to go to develop the next generation of angiogenesis inhibitors," Klauber-DeMore said.

The study was published in the current issue of The American Journal of Pathology.

More information

The U.S. National Cancer Institute has more about angiogenesis.

SOURCE: University of North Carolina at Chapel Hill, news release, April 23, 2008
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