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Carcinogenesis Advance Access originally published online on November 17, 2008
Carcinogenesis 2009 30(1):71-77; doi:10.1093/carcin/bgn258
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Polymorphisms in estrogen- and androgen-metabolizing genes and the risk of gastric cancer

Neal D. Freedman*, Jiyoung Ahn, Lifang Hou1, Jolanta Lissowska2, Witold Zatonski2, Meredith Yeager, Stephen J. Chanock, Wong Ho Chow and Christian C. Abnet

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20852, USA
1 Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
2 Department of Cancer Epidemiology and Prevention, The Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw 02-781, Poland

* To whom correspondence should be addressed. Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, 6120 Executive Boulevard, EPS/320, MSC 7232, Rockville, MD 20852, USA. Tel: +1 301 594 6119; Fax: +1 301 496 6829; Email: freedmanne{at}mail.nih.gov

Androgens and estrogens may play a role in gastric cancer etiology. To investigate the association of gastric cancer with single-nucleotide polymorphisms (SNPs) in six genes (COMT, CYP1B1, CYP17A1, CYP19A1, HSD17B1 and SHBG) involved in estrogen and androgen synthesis and metabolism, 58 haplotype-tagging SNPs were genotyped in 295 gastric cancer cases and 415 controls from a population-based study in Poland. We assessed differences in haplotype frequency between cases and controls using a global score test and calculated multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for individual haplotypes using logistic regression. We found associations in one linkage disequilibrium (LD) block containing the 3' untranslated region of COMT (rs9332377, rs165728, rs165849 and rs1110478), global score test (df = 4, P = 0.033). Relative to the most frequent GATA haplotype, the GATG haplotype was associated with statistically significant increased gastric cancer risk (OR = 1.50, 95% CI: 1.06–2.12; false discovery rate (FDR) value = 0.459) and the AACA haplotype with borderline increased risk (OR = 1.36, 95% CI = 1.00–1.85; FDR = 0.50). We also found associations for the LD block containing part of the SHBG coding region (rs6258, rs6259, rs2955617, rs1641544 and rs1641537). The CACCC haplotype was associated with statistically significant lower gastric cancer risk relative to the referent CGACC haplotype (OR = 0.55, 95% CI = 0.34–0.90; FDR = 0.459), but the overall score test was statistically non-significant. No other statistically significant associations were observed. In summary, we found possible associations between gastric cancer and polymorphisms in COMT, involved in estrogen inactivation, and SHBG, a modulator of hormone bioavailability. These findings should be interpreted cautiously until replicated in other studies.

Abbreviations: BPC3, Breast and Prostate Cohort Consortium; CI, confidence interval; FDR, false discovery rate; HW, Hardy–Weinberg; LD, linkage disequilibrium; NCI, National Cancer Institute; OR, odds ratio; SNP, single-nucleotide polymorphism; UTR, untranslated region

Received June 24, 2008; revised October 24, 2008; accepted November 13, 2008.


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