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Associations between ER, ERß, and AR Genotypes and Colon and Rectal Cancer

¹ Health Research Center and ² Department of Pathology, School of Medicine, University of Utah, Salt Lake City, Utah; ³ Fred Hutchinson Cancer Research Center, Seattle, Washington; and ⁴ Kaiser Permanente Medical Care Research Program, Oakland, California

Requests for reprints: Martha Slattery, University of Utah, 375 Chipeta Way, Suite A, Salt Lake City, UT 84108. Phone: 801-585-6955; Fax: 801-581-3623. E-mail: mslattery{at}hrc.utah.edu

Estrogen and androgens are thought to be involved in the etiology of colorectal cancer. We evaluate genetic variants of the estrogen receptor genes (ER and ERß) and the androgen receptor gene (AR). We use data from two large case-control studies of colon (n = 1,580 cases and 1,968 controls) and rectal (n = 797 cases and 1,016 controls) cancer. We evaluated the 351A>G XbaI polymorphism of ER, the 1,082 G>A and CA repeat polymorphisms of ERß, and the CAG repeat of AR. Having two 25 or more CA repeats in ERß was associated with an increased relative risk of colon cancer in women [odds ratio (OR), 2.13; 95% confidence interval (95% CI), 1.24-3.64] but not in men (P_interaction relative excess risk from interaction < 0.01; multiplicative = 0.03). Increasing number of AR CAG repeats was directly associated with colon cancer among men (OR, 1.28; 95% CI, 1.06-1.54), but not women (OR, 0.83; 95% CI, 0.68-1.02); the interaction P value for AR gene x sex was <0.01. Taking hormone replacement therapy (HRT) was associated with a reduced risk of colon cancer in the presence of the R allele of the ERß gene, whereas an R allele was associated with increased risk among postmenopausal women who did not take HRT. Postmenopausal women not using HRT who had 25 CA repeats of the ERß gene had over a 6-fold increased risk of colon cancer (OR, 6.71; 95% CI, 2.89-15.6). Our results suggest that the ERß gene is more important than ER in the etiology of colorectal cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2936–42)

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