Gene mutation protecting against malaria linked to prostate cancer incidence in African-Am...( ns that promote angiogenesis by binding...)

ns that promote angiogenesis by binding to receptors on the cells lining blood vessels adjacent to the tumor and by "attracting" them toward the tumor. This, in cooperation with the effects of other angiogenic factors, initiates new blood vessel growth towards, and ultimately into, the tumor. The DARC receptor is believed to bind to and remove angiogenic chemokines from a site of overproduction, such as inflammation or a tumor, thus limiting its ability to develop new blood vessel growth and feed itself for growth.

Breeding mice genetically engineered to develop prostate cancer to mice lacking the gene for the DARC, Drs. Lentsch and Hui Shen were able to compare growth and size of prostate cancer tumors in mice with and without the DARC.

The mice developed tumors at approximately the same time, which is not surprising, say the researchers, since chemokines have not been linked to the formation of cancer, just to its spread through angiogenesis. Once the mice's tumors formed and began to grow, however, the story was very different. In mice bred to have the mutation, and thus unable to express the chemokine-clearing DARC receptor, tumors grew much faster and were nearly four times the size of tumors, developed at the same time, in mice without the mutation. In addition, levels of angiogenic chemokines were much higher in tumors of mice without the gene for DARC.

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Contact: Sylvia Wrobel
ebpress@bellsouth.net
770-270-0989
Federation of American Societies for Experimental Biology
4-Apr-2005

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