【摘要】 [目的]研究环境暴露因素与基因多态性对肺癌发生危险性的影响。[方法]对227例原发性肺癌病人进行单纯病例研究,应用Logistic回归对CYP1A1、mEH、NAT2、NQO1、XRCC3基因多态性与多种环境危险因素之间的交互作用进行了分析。[结果]吸烟指数超过20包年者携带CYP1A1至少一个MspⅠ突变等位基因的基因型的频率高于不吸烟者(OR=1.55,95%CI=1.15~2.09;ORadj=1.39,95%CIadj=0.94~2.07)。NAT2慢代谢基因型与烹饪时厨房充满油烟味存在一定交互作用(OR=1.96,95%CI=0.95~4.07;ORadj=2.15,95%CIadj=1.01~4.57)。未发现其它代谢酶和修复酶基因与环境因素之间存在明显交互作用。[结论]携带CYP1A1MspⅠ易感基因型同时吸烟指数超过20包年,NAT2慢代谢基因型同时长期油烟暴露可能增加肺癌发生的危险性。今后应加大样本含量,进行多基因与环境因素之间的联合作用分析。更多还原

【Abstract】 Objective To explore the effects of interaction between environmental exposure factors and genetic polymorphism on the risk of lung cancer. Methods Case-only study was carried out,which involved 227 cases of primary pulmonary carcinoma. The interactions between genetic polymorphisms of CYP1A1,mEH,NAT2,NQO1 and XRCC3 and environmental exposure factors were analyzed by logistic regression model. Results The frequency of CYP1A1 genotypes carried at least one MspⅠ allele in lung cancer cases with high smoking exposure leve(lmore than 20 package years)was higher than that in cases with no smoking exposure(OR=1.55,95%CI=1.15~2.09;ORadj=1.39,95%CIadj= 0.94~2.07). There was a synergistic effect on development of lung cancer between NAT2 slow acetylator genotype and heavy oil fume in cooking(OR=1.96, 95%CI=0.95~4.07;ORadj=2.15,95%CIadj=1.01~4.57). No interactions were found between other genes and environmental exposures. Conclusion Carriers with CYP1A1 Msp Ⅰ susceptible genotype smoke more than 20 package years and carriers with NAT2 slow acetylator genotype expose to heavy oil fume for long time may increase the risk of lung cancer. A large range sample study should be performed to analyze the interactions among multi-genes and environment factors.更多还原