American Journal of Epidemiology Vol. 153, No. 9 : 851-859
Copyright © 2001 by The Johns Hopkins University School of Hygiene and Public Health
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Gene-Environment Interactions in Renal Cell Carcinoma
1 School of Community Health, College of Urban and Public Affairs, Portland State University, Portland, OR.
2 Epidemiology Division, College of Medicine, University of California at Irvine, Irvine, CA.
The majority of renal cell carcinomas (RCCs) are sporadic, and increasing incidence rates suggest that such environmental risk factors as smoking play a role in the etiology of the disease. Cases with RCC were selected from the population-based cancer registry of Orange County, California, between 1994 and 1997; controls were recruited by telephone using random digit dialing. A total of 115 case and 259 control subjects were genotyped for N-acetyltransferase 2 (NAT2), which codes for a polymorphic enzyme involved in tobacco-carcinogen metabolism. Subjects with slow acetylator genotypes were found to be at twofold increased risk (odds ratio (OR) = 1.8; 95 percent confidence interval (CI): 1.1, 2.9) of RCC. Although cancer risk doubled among smokers (OR = 2.2; 95 percent CI: 1.3, 3.7), stratified analysis revealed gene-environment interaction among slow acetylators that smoked (OR = 3.2; 95 percent CI: 1.7, 6.1) compared with rapid acetylators that smoked (OR = 1.4; 95 percent CI: 0.7, 2.9). A dose response was found for pack-years among slow acetylators (p < 0.01) but not among rapid acetylators (p = 0.06). Although smoking is a well-established risk factor of RCC, our data suggest that the risk is pronounced among slow rather than rapid acetylators.
acetyltransferases; hypertension; kidney neoplasms; smoking
Abbreviations: CI, confidence interval; NAT2, N-acetyltransferase 2 (enzyme); NAT2, N-acetyltransferase 2 (gene); OR, odds ratio; RCC, renal cell carcinoma.
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