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The 13th World Conference on Tobacco OR Health
Building capacity for a tobacco-free world
July 12-15, 2006, Washington, DC, USA
Objective: There might be integral components in the balance between carcinogen activation by enzymes (such as cytochrome 450) and detoxification, such as glutathione S-transferases (GSTs) . Numerous molecular epidemiological studies have assessed the effects of CYP1A1 genetic polymorphism and the GSTM1 deletion polymorphisms in lung cancer in recent years, yielding conflict results in various populations. The principal aims of the present study was to evaluate the role of CYP1A1 and GSTM1 genotype in lung cancer risk in relation to tobacco smoking in the North Chinese population.
Methods: The case-control study consisted of 108 primary lung cancer patients and 108 age-matched health controls from Tianjin in China. The genetic polymorphism CYP1A1 and GSTM1 were detected using the Restriction Fragment Length Polymorphism-Polymerase Chain Reaction (RELP-PCR). Logistic Regression Model was used for multivariate analysis.
Results: There were significant differences in the frequency distribution of CYP1A1 and GSTM1 polymorphisms between cases and controls groups (P<0.05). The allele frequency for CYP1A1 MSPI was 43.1% among the cases compared with 31.4% among the controls. Individuals with variant CYP1A1 genotype had a 1.89 fold increased lung cancer risk than those with wild genotype (OR=2.89, 95%CI: 1.24-6.80). The frequency of GSTM1 null genotype was higher in the case group than control group, with an OR of 1.84 (95%CI: 1.03-3.29). Multivariate analysis showed an elevated risk for lung cancer in smokers carried the variant CYP1A1 MSPI genotype and null GSTM1. Our findings supported the conclusion that CYP1A1 MSPI polymorphism, GSTM1 negative genotype are susceptibility factors of lung cancer and probably interacts with smoking.