Inflammation, infection, and prostate cancer

Purpose of review Recent evidence suggesting that inflammation and infection play a role in the etiology of prostate cancer, and the discovery of a novel virus in men with a genetic susceptibility to prostate cancer is reviewed. Recent findings Almost 20% of visceral cancers worldwide have proven infectious causes. There is substantial histologic, molecular genetic, and epidemiologic evidence that infections and inflammation are also important in the pathogenesis of prostate cancer. The R462Q allelic variant in RNASEL, an antiviral gene important in the innate immune response to viral infections, increases susceptibility to prostate cancer while resulting in vitro in deficient antiviral defenses, suggesting that prostate cancer could be caused by a virus. The study of R4620 carriers led to the discovery and biologic characterization of a novel retrovirus, xenotropic murine leukemia-related virus, isolated and cloned from prostate tissue of affected men. Biologic studies of this virus show that it is sensitive to inhibition by interferon and its downstream mediator, RNaseL, and that its DNA has integrated into the DNA of some men with prostate cancer. Summary Inflammation triggered by infection and other causes underlies the development of prostate cancer, and xenotropic murine leukemia-related virus is a candidate etiologic agent. Ongoing studies seek to define its oncogenic potential and pathogenesis.