© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 7, 545-551,
April 4, 2001
© 2001 Oxford University Press
REPORT |
Cancer Risk in Men Exposed In Utero to Diethylstilbestrol
Affiliations of authors: W. C. Strohsnitter, K. L. Noller, Department of Obstetrics and Gynecology, Tufts University School of Medicine, Boston, MA; R. N. Hoover, E. E. Hatch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; S. J. Robboy, Department of Pathology, Duke University Medical Center, Durham, NC; J. R. Palmer, Department of Epidemiology and Biostatistics, Slone Epidemiology Unit, Boston University School of Public Health, Brookline, MA; L. Titus-Ernstoff, Norris Cotton Cancer Center, Dartmouth-Hitchcock Medical Center, Lebanon, NH; R. H. Kaufman (Department of Obstetrics and Gynecology), E. Adam (Department of Epidemiology), Baylor College of Medicine, Houston, TX; A. L. Herbst, Department of Obstetrics and Gynecology, University of Chicago, IL.
Correspondence to: William C. Strohsnitter, M.S., Department of Obstetrics and Gynecology, New England Medical Center, North Bldg., 750 Washington St., Boston, MA 02111 (e-mail: wstrohsnitter{at}lifespan.org).
Background: An association between prenatal diethylstilbestrol (DES) exposure and cancer in men, especially testicular cancer, has been suspected, but findings from case–control studies have been inconsistent. This study was conducted to investigate the association between prenatal DES exposure and cancer risk in men via prospective follow-up. Methods: A total of 3613 men whose prenatal DES exposure status was known were followed from 1978 through 1994. The overall and site-specific cancer incidence rates among the DES-exposed men were compared with those of the unexposed men in the study and with population-based rates. The relative rate (RR) was used to assess the strength of the association between prenatal DES exposure and cancer development. All statistical tests were two-sided. Results: Overall cancer rates among DES-exposed men were similar to those among unexposed men (RR = 1.07; 95% confidence interval [CI] = 0.58 to 1.96) and to national rates (RR = 0.99; 95% CI = 0.65 to 1.44). Testicular cancer may be elevated among DES-exposed men, since the RRs for testicular cancer were 3.05 (95% CI = 0.65 to 22.0) times those of unexposed men in the study and 2.04 (95% CI = 0.82 to 4.20) times those of males in the population-based rates. The higher rate of testicular cancer in the DES-exposed men is, however, also compatible with a chance observation. Conclusions: To date, men exposed to DES in utero do not appear to have an increased risk of most cancers. It remains uncertain, however, whether prenatal DES exposure is associated with testicular cancer.
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