Risk of Germ Cell Tumors among Men with HIV/Acquired Immunodeficiency Syndrome

  1. James J. Goedert1,
  2. Mark P. Purdue2,
  3. Timothy S. McNeel4,
  4. Katherine A. McGlynn3,
  5. Eric A. Engels1 and
  6. for the HIV/AIDS Cancer Match Study
  1. 1Viral Epidemiology Branch, 2Occupational and Environmental Epidemiology Branch, and 3Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland and 4Information Management Services, Inc., Silver Spring, Maryland
  1. Requests for reprints:
    James J. Goedert, Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20892. Phone: 301-435-4724. E-mail: goedertj{at}mail.nih.gov

Abstract

Background: Men with HIV/acquired immunodeficiency syndrome (AIDS) are reported to be at increased risk for germ cell tumors (GCT), particularly testicular seminoma. We investigated correlates of this association to improve understanding of GCTs.

Methods: Testicular and extratesticular seminoma and nonseminoma cases were found by linking population-based cancer and HIV/AIDS registry data for 268,950 men who developed AIDS in 1980 to 2003. Standardized incidence ratios (SIR) with 95% confidence intervals (95% CI) were used to compare these cases with the number of cases expected in the demographically matched population.

Results: Overall, seminoma risk (161 cases: SIR, 1.9; 95% CI, 1.6-2.2) was increased significantly with HIV/AIDS, whereas nonseminoma risk was not (56 cases: SIR, 1.3; 95% CI, 0.96-1.7). Extratesticular GCT risk also was increased (11 cases: SIR, 2.1; 95% CI, 1.1-3.7). Seminoma risk was elevated regardless of age, race, or HIV/AIDS transmission group. It was highest for disseminated disease (SIR, 4.7; 95% CI, 2.9-7.2) and within 9 months of AIDS onset (SIR, 7.6; 95% CI, 5.8-9.6), but it was unrelated to CD4 count and duration of HIV/AIDS. The excess risk of seminoma declined in more recent calendar periods, and it was no longer elevated (SIR, 1.4; 95% CI, 0.9-1.9) in the highly active antiretroviral treatment era.

Conclusions: Men with HIV/AIDS had an increased risk of seminoma, but this risk may have attenuated with improving anti-HIV/AIDS treatments. Although detection bias could partly explain the excess of this cancer, various lines of evidence support a causal relationship. Possible mechanisms underlying this association include impaired tumor immunosurveillance or AIDS-related testicular atrophy. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1266–9)

Footnotes

  • Grant support: Intramural Research Program of the National Cancer Institute, NIH.

  • 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.

  • Note: HIV/AIDS and cancer registries in the following regions participated in the HIV/AIDS Cancer Match Study: the states of Colorado, Connecticut, Florida, Georgia, Massachusetts, Michigan, and New Jersey and the metropolitan areas of Los Angeles, San Diego, and San Francisco (California), New York City (New York), and Seattle (Washington).

    • Accepted March 16, 2007.
    • Received January 12, 2007.
    • Revision received February 28, 2007.
« Previous | Next Article »Table of Contents