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Program in Epidemiology [C. C., N. L., N. S. W., D. A. D.], Cancer Prevention Program [M. B., G. G.], and Program in Biostatistics [R. E., D. D.], Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024; Departments of Biostatistics [R. E.] and Epidemiology [C. C., N. S. W.], University of Washington, Seattle, Washington, 98195; and Swedish Tumor Institute, Seattle, Washington 98104 [G. G.]
The human androgen receptor gene contains polymorphic CAG and GGC repeats in exon 1. We investigated whether the number of CAG and/or GGC repeats is related to prostate cancer risk in a case-control study nested within the ß Carotene and Retinol Efficacy Trial. Among 300 cases and 300 controls, we did not observe any increase in risk associated with fewer CAG or GGC repeats. We observed a nonsignificant decrease in risk associated with each unit of decrease in CAG length [odds ratio (OR), 0.98; 95% confidence interval (CI), 0.931.03). Men with CAG <22 had a relative risk of prostate cancer of 0.89 (95% CI, 0.651.23) compared with men with CAG
22. There was no appreciable difference in the mean number of GGC repeats between cases and controls; the estimated change in the risk of prostate cancer associated with one fewer GGC repeat was 0.97 (95% CI, 0.881.06). The risk in men at or below the mean number of GGC repeats (17) was 0.80 (95% CI, 0.571.12). In contrast to prior reports, men with both short CAG (<22) and short GGC (
17) repeats were not at increased risk of prostate cancer (OR, 0.56; 95% CI, 0.320.98), compared with men with
22 CAG repeats and >17 GGC repeats. Our results do not support the hypothesis that a small number of CAG or GGC repeats in the androgen receptor gene increases a mans risk of prostate cancer.
Commentary
Cancer Epidemiol. Biomarkers Prev. 2002 11: 985-986.
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