Abstract
Experimental evidence has suggested that estrogen receptor alpha (coded by the gene ESR1) might increase prostate cancer risk, whereas estrogen receptor beta (coded by the gene ESR2) might reduce prostate cancer risk. We investigated the relationship with prostate cancer risk of both a TA repeat polymorphism in the ESR1 5' region, ESR1 (TA)(n), and with a CA repeat polymorphism in intron 5 of ESR2, ESR2 (CA)(n), in a case-control study (545 cases and 674 controls) nested in the Physicians' Health Study. Prostate cancer risk was highest for carriers of ESR1 (TA)(24) and ESR1 (TA)(25). Replacing one modal ESR1 (TA)(14) allele with one ESR1 (TA)(24) allele yielded an odds ratio of 1.42 (95% confidence interval, 1.00-2.00; P=0.05). Replacing one ESR1 (TA)(14) allele with one ESR1 (TA)(25) allele yielded an odds ratio of 2.10 (95% confidence interval, 1.15-3.84; P=0.02). ESR2 (CA)(n) showed no effects on prostate cancer risk. The ESR1 (TA)(n) polymorphism might play a role in prostate cancer risk.
Highlights
Effects on risk of prostate cancer of endogenous estrogens and other sex steroid hormones remain controversial
The ESR1 (TA)n polymorphism might play a role in prostate cancer risk. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2233 – 6)
Given that significant overall associations of these polymorphisms with prostate cancer risk or phenotype were not observed in prior large study [25], it is possible that we observed elevation in prostate cancer risk for carriers of ESR1 (TA)24 and ESR1 (TA)25 by chance
Summary
Effects on risk of prostate cancer of endogenous estrogens and other sex steroid hormones remain controversial. Both estrogen receptors (ER) a and h (coded by the genes ESR1 and ESR2, respectively) are expressed in human and murine prostate tissue and regulate epithelial growth [1,2,3]. Whereas ERa expression has been proposed to increase prostate cancer risk [3], recent evidence suggests that ERh expression might reduce risk by binding with an androstanediol, 5a-androstane-3h, 17h-diol [4,5,6]. Experimental evidence has suggested that estrogen receptor A (coded by the gene ESR1) might increase prostate cancer risk, whereas estrogen receptor B (coded by the gene ESR2) might reduce prostate cancer risk. Methods: We investigated the relationship with prostate cancer risk of both a TA repeat polymorphism in the ESR1 5¶ region, ESR1 (TA)n, and with a CA repeat polymorphism in intron 5 of ESR2, ESR2 (CA)n, in a case-control study (545 cases and 674 controls) nested in the Physicians’ Health Study
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