Researchers at Johns Hopkins, Wake Forest, and The National Human Genome Research Institute have implicated mutations in a “heart disease gene” in hereditary prostate cancer. The findings, which offer new evidence that at least some cases of prostate cancer may begin with an infection and inflammatory response, will be published online September 16, 2002, in Nature Genetics.
The gene, called macrophage scavenger receptor-1 (MSR1), was identified more than 20 years ago as a factor in plaque formation in arteries, a process that contributes to coronary artery disease, or so-called hardening of the arteries. MSR1 helps immune system cells called macrophages clean up cellular debris from bacterial infections and damaged fats or lipids. Macrophage activity has been known to increase in the early stages of prostate cancer, and the Hopkins investigators suspected that some MSR1 mutations might inhibit the ability of macrophages to clean up properly after prostate infections, producing inflammatory lesions that are often markers of prostate cancer.
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