Carcinogenesis Advance Access originally published online on March 25, 2004
Carcinogenesis 2004 25(8):1395-1401; doi:10.1093/carcin/bgh153
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Carcinogenesis vol.25 no.8 © Oxford University Press 2004; all rights reserved.
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Gene–environment interactions between the smoking habit and polymorphisms in the DNA repair genes, APE1 Asp148Glu and XRCC1 Arg399Gln, in Japanese lung cancer risk
1 Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya Aichi, 2 Department of Internal Medicine and Molecular Science, Nagoya City University, Graduate School of Medical Sciences, Nagoya Aichi, 3 Department of Preventive Medicine, Biostatistics and Medical Decision Making, Nagoya Graduated School of Medicine, Nagoya Aichi, 4 Department of Thoracic Surgery, Aichi Cancer Center Hospital, Nagoya Aichi, 5 Department of Thoracic Oncology, Aichi Cancer Center Hospital, Nagoya Aichi, 6 Division of Clinical Laboratories, Aichi Cancer Center Hospital, Nagoya Aichi, Japan and 7 Department of Preventive Medicine, General Surgery and Cancer Research Institute, Seoul National University, Seoul, South Korea
8 To whom correspondence should be addressed Email: hidemi{at}aichi-cc.jp
APE1 (apurinic/apyrimidinic endonuclease 1) and XRCC1 (X-ray cross-complementing group 1) are DNA repair proteins that play important roles in the base excision repair (BER) pathway. Polymorphisms in their encoding genes are associated with altered DNA repair capacity and thus may impact on cancer risk. In the present case-control study with 178 Japanese incident lung cancer cases and 449 age- and sex-matched controls, we investigated the gene–environment interaction among APE1 Asp148Glu, XRCC1 Arg399Gln and smoking habit in lung cancer risk. The results were analyzed by using conditional logistic regression models, adjusted for age, sex and smoking status. The adjusted odds ratio for the current smokers with APE1 148Asp/Asp, Asp/Glu and Glu/Glu genotype as compared with the never smokers with the Asp/Asp genotype were 3.01 (95% CI 1.39–6.51, P = 0.005), 2.73 (95% CI 1.29–5.77, P = 0.008) and 7.33 (95% CI 2.93–18.3, P < 0.001), respectively. The gene–environment interaction between current smoking and APE1 148Glu/Glu genotype was statistically significant (OR 3.59, 95% CI 1.28–10.1, P = 0.015). When APE1 Asp148Glu and XRCC1 Arg399Gln polymorphisms were evaluated together, the adjusted odds ratios for the current smokers with 0–1, 2 and 3–4 of APE1 148Glu or XRCC1 399Gln alleles as compared with never smokers with the 0 of these alleles were 2.96 (95% CI 1.57–5.58, P = 0.001), 3.86 (95% CI 1.85–8.05, P < 0.001) and 6.01 (95% CI 2.25–16.1, P < 0.001), respectively. The gene–environment interaction between current smoking and three or more APE1 148Glu or XRCC1 399Gln alleles was statistically significant (OR 2.44, 95% CI 1.00–9.22, P = 0.049). The OR for the gene–environment interaction of Glu/Glu genotype of APE1 codon 148 with heavy smoking was 1.04 (95% CI 0.38–2.90, P = 0.936) and that with light smoking was 2.67 (95% CI 1.00–7.68, P = 0.049). These results suggest that APE1 Asp148Glu and XRCC1 Arg399Gln polymorphisms might modify the risk of lung cancer attributable to cigarette smoking exposure.
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