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Glutathione Transferase (GSTM1) Null Genotype, Smoking, and Prevalence of Colorectal Adenomas¹

Department of Pediatrics, Division of Medical Genetics, Harbor-University of California-Los Angeles Medical Center, Torrance, California 90502 [H. J. L., C-Y. H., B. K. L., D. B. L.]; Department of Epidemiology, University of California-Los Angeles School of Public Health, Los Angeles, California 90024 [N. M. P-H., M. P. L.]; Department of Gastroenterology, Kaiser Permanente, Los Angeles, California 90027 [H. D. F.] and Bellflower, California 90706 [E. R. L]; and Department of Preventive Medicine, University of Southern California School of Medicine, Los Angeles, California 90033 [N. M. P-H., S. A. I., M. P. L., R. W. H.]

Colorectal cancer is caused by environmental exposures and genetic predisposition. However, little is known of hereditary factors that influence development of common, non-Mendelian forms of this cancer. Interactions among carcinogen exposure, hereditary variants of enzymes involved in carcinogen metabolism, and other host factors may play a role. Genetic polymorphisms of carcinogen metabolism, such as the glutathione transferase M1 (GSTM1) null genotype, are thus possibly related to cancer risk. The GSTM1 enzyme detoxifies mutagens formed from polycyclic aromatic hydrocarbons which are found in tobacco smoke. We analyzed GSTM1 genotypes and smoking among 488 controls and 446 individuals with a first time diagnosis of colorectal adenomas which are precursors to cancer. Subjects were from two Kaiser Permanente sigmoidoscopy clinics in southern California. We observed no overall effect of the GSTM1 null genotype on the risk for colorectal adenomas (odds ratio, 0.85; 95% confidence interval = 0.65–1.10). The odds ratio for smokers with the null genotype was 2.07 (95% confidence interval = 1.14–3.77) when compared to "never smokers" without the null genotype. Using this same reference group, the odds ratio for smokers without the null genotype was 1.73 (95% confidence interval = 1.03–2.90). These two odds ratios were not significantly different (P = 0.30).

¹ H.J.L. was supported by grants from the University of California-Los Angeles Clinical Nutrition Research Unit, the Cancer Research Foundation of America, the March of Dimes (Basil O'Connor Awards 5-FY92-1216 and 5-FY93-0995), American Cancer Society Institutional Grant IN/IRG 131N to the Jonsson Comprehensive Cancer Center at University of California-Los Angeles, the University of California Cancer Research Coordinating Committee, the Wendy Will Case Cancer Fund, and the Harbor Collegium at Harbor-University of California-Los Angeles Medical Center. N. M. P-H. was supported by the Swiss League Against Cancer, and R. W. H. was supported by National Cancer Institute Grants 1R01CA51923 and 1R01CA63699.

² To whom requests for reprints should be addressed, at Division of Medical Genetics, E4, Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502.

Received 12/ 9/94. Accepted 2/ 2/95.

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