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目的:探讨被动吸烟人群尼古丁受体3基因(CHRNA3)启动子区遗传变异与肺癌发病的关系。方法:用病例-对照的研究方法,收集250例被动吸烟原发性肺癌患者和250例性别相同、年龄相差±1岁被动吸烟正常对照,采用PCR-RFLP技术检测CHRNA3基因启动子单核苷酸多态位点rs6495309(T>C)的基因型,用SAS 9.13软件进行非条件Logistic回归校正混杂因素的影响,分析基因变异与肺癌发病的关联。结果:基因型频率分析均符合Hardy-Weinberg平衡,P=0.109 6;CHRNA3 rs6495309(T>C)位点变异在肺癌与对照中的分布差异有统计学意义,P=0.043 2;携带CC基因型个体发生肺癌的危险性较TT基因型个体增加81%(95%CI=1.07～3.06;P=0.019);rs6495309C变异基因型(rs6495309TC和rs6495309CC)患肺癌的危险性增加(adjusted OR=1.63;95%CI=1.06～2.50;P=0.025)。发现被动吸烟来自于父母人群时该位点变异在肺癌与对照中分布差异有统计学意义,P=0.047 9。结论:CHRNA3基因启动子rs6495309(T>C)变异的被动吸烟人群肺癌发病危险性较高,且其危害性主要表现为被动吸烟来源于父母的人群。
Objective: To investigate the relationship between genetic variation of the promoter region of nicotine receptor 3 (CHRNA3) gene and the pathogenesis of lung cancer in passive smoking population. METHODS: A case-control study was conducted in 250 patients with passive smoking primary lung cancer and 250 normal controls of the same gender with a mean of ± 1 year old passive smoking. PCR-RFLP was used to detect the single nucleotide of CHRNA3 promoter The polymorphism rs6495309 (T> C) genotypes were analyzed using SAS 9.13 non-conditional logistic regression to correct for confounding factors and to analyze the association between genetic variation and lung cancer incidence. Results: The frequencies of genotypes were in accordance with Hardy-Weinberg equilibrium (P = 0.109 6). There was significant difference in the distribution of CHRNA3 rs6495309 (T> C) locus between lung cancer and controls (P = 0.043 2) The risk of developing lung cancer was 81% (95% CI = 1.07-3.06; P = 0.019) in individuals with TT genotype. The risk of lung cancer was increased in rs6495309C and rs6495309CC patients (adjusted OR = 1.63; 95 % CI = 1.06 ~ 2.50; P = 0.025). Found that passive smoking from the parent population at this site mutation in lung cancer and control distribution was statistically significant, P = 0.047 9. Conclusion: The risk of lung cancer is high in passive smoking population of rs6495309 (T> C) mutation of CHRNA3 gene promoter, and its harmfulness is mainly manifested by the population of passive smoking originating from parents.