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Sexually Transmissible Infections and Prostate Cancer Risk

¹ Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland; ² Stanley Division of Developmental Neurovirology, Johns Hopkins University School of Medicine, Baltimore, Maryland; ³ Division of Infectious Diseases, Epidemiology, and Immunology, Emory University School of Medicine; ⁴ Department of Pathology and Laboratory Medicine, Emory University School of Medicine and Grady Memorial Hospital; ⁵ Chlamydia Laboratory, Centers for Disease Control and Prevention, Atlanta, Georgia; ⁶ Marshfield Clinic Research Foundation, Marshfield, Wisconsin; and ⁷ Viral Oncology Section, AIDS Vaccine Program, Science Applications International Corporation-Frederick, National Cancer Institute-Frederick, Frederick, Maryland

Requests for reprints: Wen-Yi Huang, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, 6120 Executive Boulevard, EPS 8110, MSC 7240, Bethesda, MD 20892. Phone: 301-435-4710; Fax: 301-402-1819. E-mail: huangw{at}mail.nih.gov

Background: Sexually transmissible infections (STI) have been variably associated with increased risks of prostate cancer, largely in case-control studies.

Methods: In the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we examined risk of prostate cancer in relation to serum antibodies to Chlamydia trachomatis, human papillomavirus-16 and -18, herpes simplex virus-2, cytomegalovirus, and human herpesvirus-8 in 868 cases (765 Whites and 103 Blacks) and 1,283 controls matched by race, age, time since initial screening, and year of blood draw; all blood samples were collected at least 1 year before prostate cancer diagnosis, except for 43 Black cases. We also assessed risk associated with self-reported history of syphilis and gonorrhea.

Results: Prevalences of the 7 STIs among controls were weakly correlated, and all were more frequent among Blacks than Whites, except for human herpesvirus-8. Among Whites, prostate cancer risk was not significantly associated with the individual infections or with their number (P_trend = 0.1); however, men with one or more STI had slightly higher risk (odds ratio, 1.3; 95% confidence interval, 1.0-1.6). Among Blacks, excess risk was associated with IgA antibody to C. trachomatis (odds ratio, 2.1; 95% confidence interval, 1.2-3.6).

Conclusion: This large prospective study of prostate cancer shows no consistent association with specific STIs and a borderline association with any versus none. Whether a shared response or correlated infection not directly measured underlies the weak association requires further study. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2374–81)