论文部分内容阅读
[目的]研究P16基因甲基化、谷胱甘肽硫转移酶M1基因(GSTM1)多态性和环境暴露与非小细胞肺癌(NSCLC)的关系。[方法]采用病例对照研究方法选择47例NSCLC患者和94例对照,用甲基化特异性PCR(MSP)检测P16基因甲基化,GSTM1基因多态性用限制性片断长度多态性PCR(PCR-RFLP)测定。[结果]肺癌组接触粉尘、毒物频率高于对照组(P﹤0.01),食用蔬菜水果、饮用消毒水频率肺癌组低于对照组(P﹤0.01);肺癌组织甲基化率44.7%,高于癌旁组织的17%(P﹤0.01),甲基化和吸烟高度相关(P﹤0.01);GSTM1多态性分布无统计学意义(P﹥0.05),粉尘接触、吸烟和GSTM1缺陷型有协同作用,P16甲基化和GSTM1多态性关系不明显。[结论]接触粉尘、毒物明显增加NSCLC危险性,食用蔬菜水果和消毒水降低NSCLC危险性;吸烟致P16基因甲基化参与NSCLC的形成,粉尘、吸烟可能增加GSTM1缺失型患NSCLC危险性,未发现P16甲基化和GSTM1多态性有交互作用。
[Objective] To investigate the relationship between P16 gene methylation, glutathione S-transferase M1 gene (GSTM1) polymorphism and environmental exposure and non-small cell lung cancer (NSCLC). [Methods] 47 cases of NSCLC patients and 94 controls were selected by case-control study. The methylation of P16 gene was detected by methylation-specific PCR (MSP), and the polymorphism of GSTM1 gene was analyzed by restriction fragment length polymorphism PCR PCR-RFLP) assay. [Results] The frequency of exposure to dust and poison in lung cancer group was higher than that in control group (P <0.01). The frequency of eating fruits and vegetables and drinking disinfection water in lung cancer group was lower than that in control group (P <0.01). The methylation rate of lung cancer tissue was 44.7% (P <0.01). The methylation and smoking were highly correlated (P <0.01). The distribution of GSTM1 polymorphism was not statistically significant (P> 0.05). Dust exposure, smoking and GSTM1 deficient Synergy, P16 methylation and GSTM1 polymorphism is not obvious. [Conclusion] The exposure to dust and poison obviously increased the risk of NSCLC. The consumption of vegetables and fruits and disinfectant water reduced the risk of NSCLC. The methylation of P16 gene in NSCLC caused by smoking was involved in the formation of dust and smoking, and the risk of NSCLC in GSTM1 deletion was increased. P16 methylation was found to interact with GSTM1 polymorphism.