© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 24, 2009-2017,
December 20, 2000
© 2000 Oxford University Press
Racial Variation in Prostate Cancer Incidence and in Hormonal System Markers Among Male Health Professionals
Affiliations of authors: E. A. Platz, Department of Nutrition, Harvard School of Public Health, Boston, MA; E. B. Rimm, W. C. Willett, E. Giovannucci, Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, and the Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston; P. W. Kantoff, Lank Center for Genitourinary Oncology, Department of Adult Oncology, Dana-Farber Cancer Institute, Harvard Medical School.
Correspondence to present address: Elizabeth A. Platz, Sc.D., M.P.H., Department of Epidemiology, The Johns Hopkins School of Hygiene and Public Health, 615 N. Wolfe St., Baltimore, MD 21205 (e-mail: eplatz{at}jhsph.edu).
Background: Racial variation in prostate cancer incidence in the United States is pronounced, with African-American men having the highest rates. Whether differences in the distribution of known or suspected risk factors among racial groups explain this variation is unknown. Methods: We evaluated prospectively the relation between prostate cancer and race among 45 410 U.S. male health professionals aged 40–75 years in 1986. We used multivariable, pooled logistic regression to adjust the rate ratio (RR) for potential dietary and lifestyle risk factors. We also measured circulating levels of steroid hormones, sex hormone-binding globulin, and vitamin D metabolites and length of the androgen receptor gene CAG repeat in a sample of African-American (n = 43), Asian (n = 52), and white (n = 55) participants and assessed variation by race in these possible prostate epithelial cell growth mediators by use of analysis of variance. Statistical tests were two-sided. Results: The age-adjusted RR for prostate cancer was 1.73 (95% confidence interval [CI] = 1.23–2.45) for African-American men compared with white men. After multivariate adjustment, the RR increased to 1.81 (95% CI = 1.27–2.58). The rate of prostate cancer did not differ between Asians and whites. Steroid hormone and 1,25-dihydroxyvitamin D levels did not vary appreciably by race. However, the mean number of androgen receptor gene CAG repeats was lower among African-Americans (mean ± standard deviation = 20.1 ± 3.5) than among whites (22.1 ± 3.1; P = .007) and Asians (22.1 ± 3.9; P = .009). Conclusions: Our results confirm the elevated incidence of prostate cancer among African Americans and show that it is not explained by differences in the distribution of possible dietary and lifestyle risk factors in this cohort. Racial variation in length of the androgen receptor gene CAG repeat may explain a small part of the excess risk of prostate cancer among African-American men in this cohort.
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