Serologic Evidence of Human Papillomavirus 16 and 18 Infections and Risk of Prostate Cancer1

  1. Karin A. Rosenblatt,
  2. Joseph J. Carter,
  3. Lori M. Iwasaki,
  4. Denise A. Galloway and
  5. Janet L. Stanford2
  1. Department of Community Health, University of Illinois at Urbana-Champaign, Champaign, Illinois 61820 [K. A. R.], and Program in Cancer Biology, Division of Human Biology [J. J. C., D. A. G.] and Program in Epidemiology, Division of Public Health Sciences [L. M. I., J. L. S.], Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024

    Abstract

    Human papillomavirus (HPV) subtypes 16 and 18 are sexually transmitted and have been associated with an increased incidence of several anogenital tumors. Although previous epidemiological studies have suggested that sexual behaviors such as an early age at first intercourse and larger numbers of sexual partners are also related to an increased risk of prostate cancer, seroepidemiological studies of these infectious agents in relation to prostate cancer have produced differing results. To further evaluate this potential relationship, we completed a population-based control study in King County, Washington. Middle-aged (40–64 years) men diagnosed with prostate cancer (n = 642) were ascertained through the Seattle-Puget Sound Surveillance, Epidemiology, and End Results cancer registry between January 1993 and December 1996. Controls (n = 570) of similar age were selected from the same population as the cases by random digit dialing. Overall, there was no association between serological evidence of prior HPV-16 (adjusted odds ratio, 1.06; 95% confidence interval, 0.71–1.57) or HPV-18 (adjusted odds ratio, 1.36; 95% confidence interval, 0.69–2.69) infection and the risk of prostate cancer. Analyses of clinical features demonstrated no relationship between HPV infection status and Gleason score, stage of disease, or a combined measure of disease aggressiveness. Our findings indicate that HPV-16 and HPV-18 are not associated with prostate cancer risk.

    Footnotes

    • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • 1 Supported by Grants CA56678 and CA92777 and Contract NO1-CN-05230 from the National Cancer Institute, NIH, Department of Health and Human Services.

    • 2 To whom requests for reprints should be addressed, at Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, MW-814 Seattle, WA 98109-1024. Phone: (206) 667-2715; Fax: (206) 667-2717; E-mail: jstanfor{at}fhcrc.org

    • 3 The abbreviations used are: OR, odds ratio; CI, confidence interval; HPV, human papillomavirus; PSA, prostate-specific antigen.

      • Accepted May 7, 1903.
      • Received December 30, 1902.
      • Revision received May 2, 1903.
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