Sexually transmissible infections and prostate cancer risk

Sexually transmissible infections and prostate cancer risk - Circulating antibodies against infectious agents and self-reported history of syphilis and gonorrhea represent an individual's cumulative lifetime exposure or past infections, and thus are particularly suited for risk evaluation of cancer with a long latent disease process. Our analysis examining serology of Chlamydia trachomatis, human papillomavirus (HPV) types 16 and 18, herpes simplex virus (HSV) type 2, cytomegalovirus (CMV), and human herpes virus 8 (HHV-8), and self-reported history of syphilis and gonorrhea, is among the first to examine the effects of many sexually transmissible infections (STIs) simultaneously in a large prospective study of prostate cancer risk. We found no strong association between prior evidence of specific STIs and prostate cancer, but having had any of the 7 STIs was associated with a modestly increased risk among whites. In the smaller number of black men studied, we found an increased risk associated with IgA antibody to C. trachomatis, and a non-significant elevation with 2 or more prior STIs.

Other infections were linked with increased prostate cancer risk in previous studies, including seropositivity for Trichomonas vaginalis, long-term use of tetracycline, an antibiotic used to treat severe acne, and a novel retrovirus named XMRV discovered in prostate cancer tissues from men carrying genetic variants of RNASEL. A potential explanation for these disparate associations is that the host response of infection, specifically inflammation, represents a final common pathway for prostate cancer risk. Chronic inflammation as a potential mechanism of prostate carcinogenesis is supported by several lines of evidence, including activated inflammatory cells frequently found in prostate cancer tissues, genetic and circulating markers of inflammation and host response to infection variably shown to increase prostate cancer risk, and intake of NSAIDs and antioxidants found to be protective. Alternatively, the diffuse associations with the various infections may be due to correlation with a true causal factor not directly measured.

In summary, this large prospective study found no consistent association between history of individual STIs and prostate cancer risk. Our novel finding of an increased risk with C. trachomatis IgA antibodies was restricted to blacks and requires confirmation. By studying many STIs simultaneously, we found a modest risk associated with any prior STI among whites. The modest associations and lack of specificity parallel the variable findings from previous reports and may suggest involvement of a correlated factor or shared underlying response (e.g. inflammation) not directly measured. Further studies in high-risk populations would help advance our understanding of the role of STIs in the etiology of prostate cancer.

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