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Endogenous Hormones and Prostate Cancer Collaborative Group. Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies [abstract]. J Natl Cancer Inst 2008; 100:170-183. Pooled analysis of 18 prospective studies (total of 3886 prostate cancer cases and 6438 controls) on serum androgens and prostate cancer risk showed no association between total androgen levels and disease risk. A suggestive inverse relationship between serum SHBG levels and prostate cancer risk was observed.
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Weiss JM, Huang WY, Rinaldi S, et al. Endogenous sex hormones and the risk of prostate cancer: a prospective study. Int J Cancer 2008 [Epub ahead of print]. In a population of 727 incident Caucasian prostate cancer cases and 889 matched controls nested in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial, prostate cancer risks were not associated with serum androgens or SHBG. There was an observed increase in prostate cancer risk with increasing testosterone-to-SHBG ratio, which was restricted mainly to risk in older men (-≥65 years) and particularly for aggressive disease.
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Sarma AV, Dunn RL, Lange LA, et al. Genetic polymorphisms in CYP17, CYP3A4, CYP19A1, SRD5A2, IGF-1, and IGFBP-3 and prostate cancer risk in African-American men: the Flint Men's Health Study. Prostate 2008; 68:296-305. In a population of African-Americans in the Flint Men's Health Study (131 cases and 342 controls), variations in CYP17, CYP3A4, CYP19A1, SDR5A2, IGF1, and IGFBP3 were assessed for associations with prostate cancer. Three of four variants in CYP17 were associated with prostate cancer risk; all three variants reside in exons or at the 50 untranslated region.
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n repeat polymorphism within the third intron was associated with increased risk for prostate cancer among all patients and Caucasians but not in African-Americans. Also, no associations were seen for the SRD5A2 V89L variation. Most of the prostate cancer risk associated with the intron 3 HSD3B2 short allele was confined to the SRD5A2 89L variant subgroup and indicated that in combination these polymorphisms may be associated with an increased risk of aggressive disease (Gleason >7).
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