NAT2 slow acetylator genotype is associated with increased risk of lung cancer among non-smoking Chinese women in Singapore

Authors: Lee E.J.D.1; Zhao B.1; Poh W-T.4; Teh M.2; Eng P.5; Wang Y-T.6; Tan W-C.3; Seow A.; Lee H-P.

Source: Carcinogenesis, Volume 20, Number 9, September 1999 , pp. 1877-1881(5)

Publisher: Oxford University Press

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Abstract:

Among non-smokers, the factors resulting in lung carcinogenesis are poorly understood. We conducted a hospital-based case-control analysis of 294 Chinese women, of whom 217 were non-smokers, to evaluate the role of polymorphic N-acetyltransferase (NAT2) as a susceptibility factor for the disease. The proportion of slow acetylator genotypes among non-smoking cases (n = 92) and controls (n = 125) was 38.0 and 24.0%, respectively [odds ratio (OR) 2.0, 95% confidence interval (CI) 1.1–3.7]. No effect of NAT2 genotype was seen among smokers. Among non-smokers, the effect was marked for adenocarcinomas (OR 2.1, 95% CI 1.1–4.0). As NAT2 activity is known to modify risk of arylamine-induced carcinogenesis, our results suggest that exposure to arylamines in the environment may play a role in risk of lung cancer among non-smokers.

Document Type: Original article

Affiliations: Department of Community, Occupational and Family Medicine, Faculty of Medicine, National University of Singapore, 16 Medical Drive, Singapore, 117597, : 1: Department of Pharmacology, 2: Department of Pathology and 3: Department of Medicine, Faculty of Medicine, National University of Singapore, Lower Kent Ridge Road, Singapore, 119260, 4: Department of Pathology and 5: Department of Respiratory and Critical Care Medicine, Singapore General Hospital, Outram Road, Singapore, 169608 and 6: Department of Respiratory Medicine, Tan Tock Seng Hospital, Moulmeri Road, Singapore 308433

Publication date: 1999-09-01

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  • Carcinogenesis is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal will publish papers that warrant prompt publication in the areas of Cancer Biology, Molecular Epidemiology and Cancer Prevention, and Carcinogenesis.
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