Gene-environment interactions in renal cell carcinoma

Citation
Jc. Semenza et al., Gene-environment interactions in renal cell carcinoma, AM J EPIDEM, 153(9), 2001, pp. 851-859
Citations number
39
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Envirnomentale Medicine & Public Health","Medical Research General Topics
Journal title
AMERICAN JOURNAL OF EPIDEMIOLOGY
ISSN journal
0002-9262 → ACNP
Volume
153
Issue
9
Year of publication
2001
Pages
851 - 859
Database
ISI
SICI code
0002-9262(20010501)153:9<851:GIIRCC>2.0.ZU;2-F
Abstract
The majority of renal cell carcinomas (RCCs) are sporadic, and increasing i ncidence rates suggest that such environmental risk factors as smoking play a role in the etiology of the disease. Cases with RCC were selected from t he population-based cancer registry of Orange County, California, between 1 994 and 1997; controls were recruited by telephone using random digit diali ng. A total of 115 case and 259 control subjects were genotyped for N-acety ltransferase 2 (NAT2), which codes for a polymorphic enzyme involved in tob acco-carcinogen metabolism. Subjects with slow acetylator genotypes were fo und to be at twofold increased risk (odds ratio (OR) = 1.8; 95 percent conf idence 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 g ene-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). Alt hough smoking is a well-established risk factor of RCC, our data suggest th at the risk is pronounced among slow rather than rapid acetylators.