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Dietary Selenium Intake and Genetic Polymorphisms of the GSTP1 and p53 Genes on the Risk of Esophageal Squamous Cell Carcinoma

¹ Department of Epidemiology, School of Public Health, and ² Center for Human Nutrition, School of Medicine, University of California at Los Angeles; ³ Center for Craniofacial Molecular Biology, University of Southern California, Los Angeles, California; ⁴ Department of Epidemiology, Fujian Medical University, Fuzhou, Fujian, China; ⁵ Department of Epidemiology, Fudan University School of Public Health; ⁶ Shanghai Pudong CDC, Shanghai, China; ⁷ Department of Chronic Disease Prevention, Jiangsu CDC, Nanjing, China; ⁸ Taixing City Center for Disease Prevention and Control, Taixing, Jiangsu, China; and ⁹ Roswell Park Cancer Institute, Buffalo, New York

Requests for reprints: Zuo-Feng Zhang, Department of Epidemiology, School of Public Health, University of California at Los Angeles, 71-225 CHS, Box 951772, 650 Charles Young Drive, Los Angeles, CA 90095-1772. Phone: 310-825-8418; Fax: 310-206-6039. E-mail: zfzhang{at}ucla.edu

Few studies have assessed potential effect modifications by polymorphisms of susceptibility genes on the association between selenium intake and esophageal squamous cell carcinoma (ESCC). We studied the joint effects of dietary selenium and the GSTP1 and p53 polymorphisms on ESCC risk in a population-based case-control study with 218 ESCC cases and 415 controls in Taixing City, China. Dietary selenium intake was estimated from a food frequency questionnaire with 97 food items. GSTP1 and p53 polymorphisms were detected by RFLP-PCR assays. Logistic regression analyses were done to estimate odds ratios (OR) and 95% confidence intervals (95% CI). Reduced ESCC risk was observed among individuals in the highest quartile of dietary selenium intake (adjusted OR, 0.31; 95% CI, 0.13-0.70) with a dose-dependent gradient (P_trend = 0.01). The p53 Pro/Pro genotype was associated with increased risk of ESCC compared with the Arg/Arg genotype (adjusted OR, 2.02; 95% CI, 1.19-3.42). When combined with selenium consumption, an obvious increased risk was observed among individuals with the p53 Pro/Pro or GSTP1 Ile/Ile genotype with adjusted ORs of 3.19 (95% CI, 1.74-5.84) and 1.90 (95% CI, 1.03-3.51), respectively. Among smokers and alcohol drinkers, elevation of ESCC risk was more prominent among p53 Pro/Pro individuals who consumed a low level of dietary selenium (adjusted OR, 3.59; 95% CI, 1.49-8.66 for smokers and 6.19; 95% CI, 1.83-20.9 for drinkers). Our study suggests that the effect of dietary selenium on the risk of ESCC may be modulated by tobacco smoking, alcohol drinking, and p53 Pro/Pro and GSTP1 Ile/Ile genotypes. (Cancer Epidemiol Biomarkers Prev 2006;15(2):294–300)

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