Human papillomavirus DNA in malignant and hyperplastic prostate tissue of black and white males.

Abstract

Prostate adenocarcinoma is the most common cancer in U.S. males with incidence rates in African-Americans 40% higher than in whites. While etiology is poorly understood, several studies have hypothesized that infection with human papillomavirus (HPV) is a risk factor. This study hypothesized that HPV infection is associated with increased prostate cancer risk, and a higher prevalence of oncogenic viral DNA is responsible for greater risk in African-Americans. Archival tissues from 42 pairs of subjects (one with prostatic adenocarcinoma (cases) and one with benign prostatic hyperplasia (controls)) matched by race and age, and an additional 20 unmatched black cases were tested for HPV DNA. Viral L1 and E6 gene sequences were amplified by polymerase chain reaction (PCR) and electrophoresed on polyacrylamide gels. Positive L1 PCR products were further screened for HPV DNA by hybridization using specific probes internal to the amplified region and relative risks of prostate cancer in HPV positive and negative individuals determined. Positive samples were hybridized to type-specific E6 probes of HPV 6, 11, 16, 18, 31, 33 or 45. After excluding 6 cases with inconclusive hybridization screening results, 7 of 56 (12.5%) cases were HPV positive compared to 4 of 42 (9.5%) controls. Four of 52 (7.7%) blacks were positive compared to 7 of 46 (15.2%) whites. The odds ratio for being positive in blacks vs. whites was 0.46 (95% confidence interval = 0.13, 1.70). The crude odds ratio for prostate cancer in HPV positive individuals was 1.36 (0.37, 4.98). The age/race-adjusted odds ratio was 1.66 (0.33, 8.37). Matched pairs analysis yielded an odds ratio of 3.00 (0.61, 14.86). None of the positive samples hybridized to the type-specific E6 probes. HPV did not emerge as a significant risk factor for prostate cancer. These results may be influenced by small sample size and measurement error. The lower prevalence in blacks suggests that excess prostate cancer risk is not explained by HPV infection, unless future research reveals more highly oncogenic types in blacks. Since HPV was found in both cases and controls, virus typing may reveal an association not apparent in the present studies.