| Titre : | Gene-environment interactions in renal cell carcinoma. (2001) |
| Auteurs : | Jan-C SEMENZA ; Hoda ANTON-CULVER ; Joan LARGENT ; David PEEL ; Argyrios ZIOGAS ; Epidemiology Division. College of Medicine. University of California at Irvine. Irvine. CA. USA |
| Type de document : | Article |
| Dans : | American journal of epidemiology (vol. 153, n° 9, 2001) |
| Pagination : | 851-859 |
| Langues: | Anglais |
| Mots-clés : | Cancer ; Rein ; Tabagisme ; Génétique ; Enzyme ; Epidémiologie ; Facteur risque ; Homme ; Etats Unis ; Amérique ; Registre ; Appareil urinaire [pathologie] ; Rein [pathologie] ; Amérique du Nord |
| Résumé : | [BDSP. Notice produite par INIST 2Qzf5R0x. Diffusion soumise à autorisation]. 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 (Cl) : 1.1,2.9) of RCC. Although cancer risk doubled among smokers (OR=2.2 ; 95 percent Cl : 1.3,3.7), stratified analysis revealed gene-environment interaction among slow acetylators that smoked (OR=3.2 ; 95 percent Cl : 1.7,6.1) compared with rapid acetylators that smoked (OR=1.4 ; 95 percent Cl : 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. |
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