Gene mutation protecting against malaria linked to prostate cancer incidence in African-American men

A University of Cincinnati College of Medicine suggests that the 60 percent greater incidence of prostate cancer among African-American men is related to a gene mutation developed generations ago in West Africa as nature's way of providing protection from the malaria infection endemic in that part of the world. Approximately 70 percent of African-Americans have the mutation. The preclinical study was presented Tuesday, April 5, at the American Society of Investigative Pathology sessions of Experimental Biology 2005.

The gene mutation prevents expression of the Duffy antigen/receptor for chemokines (DARC) on red blood cells. The DARC originally was described by scientists as a red blood cell receptor required for infection by the malarial parasite. More recent evidence, however, suggests that the DARC may also play a role in preventing or slowing the formation of new blood vessels produced by tumors in order to gain nutrients needed to grow.

Dr. Alex B. Lentsch says this is an important first step towards identifying a causative factor for the higher prevalence of prostate cancer in African-American men as well as their two-fold higher mortality than white men. His study suggests that prostate cancer in men with a mutated DARC gene would develop more quickly to the level of detection and grow more aggressively.

These pre-clinical studies will need to be validated in prostate cancer patients, he adds. But once that is done, a simple blood test measuring the presence or absence of the DARC on red blood cells could be used to identify prostate cancer patients at higher risk for aggressive growth of the tumor. It is also possible that anti-chemokine therapies could be tested and applied to these patients.

Tumor angiogenesis occurs when tumor cells release small compounds or angiogenic factors that cause existing blood vessels to grow into the tumor. One class of angiogenic factors released by prostate tumors are chemokines, small protei

Contact: Sylvia Wrobel
Federation of American Societies for Experimental Biology

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