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目的探讨谷胱甘肽转移酶(GST)和细胞色素CYP1A1、CYP2E1多态性与肺癌易感性的关系。方法用病例对照研究方法,收集广东籍新发原发性肺癌病人91例及同期非肺部疾患住院病人91例作对照,采用聚合酶链式反应(PCR)和限制性片段长度多态性(RFLP)技术检测病例和对照的CYP1A1、CYP2E1和GSTM1基因多态性。结果CYP1A1突变型(m2m2)与野生型(mlml)比较,OR值1.51;CYP2E1C1C1型与C1C2型比较,OR值1.80;C2C2型与C1C2型比较,OR值5.48;GSTM1基因缺失型与正常型比较;OR值1.26。两种基因联合分析结果表明:GSTM1基因缺失并携带CYPlAlm2m2与GSTM1基因正常并携带CYP1A1m1m1者比较,OR值2.29,GSTM1基因缺失并携带CYP2E1C1C1型者与GSTM1基因正常并携带CYP2E1C1C2型者比较,OR值2.13,携带CYP1A1m2m2型以及CYP2E1C1C1型者与携带CYP1A1m1m1型和CYPE1c1c2型者比较,OR值3.00。3种基因联合作用分析结果表明:携带CYP1A1m2m2型以及CYP2E1C1C1型并且GSTM1基因缺失者比携带CYP1A1m1m1型和CYP2E1c1c2型且GSTM1基因正常者提高了患肺癌的危险性,OR值3.97。结论CYP1A1、CYP2E1和GSTM1在单因素分析中末显示出与肺癌风险的联系,2个基因和3种基因的联合作用似乎可以提高患肺癌的危险性,但无统计学意义。提示这3种基因均不是肺癌个体易感性的主效基因,可能是次效基因。
Objective To investigate the relationship between glutathione transferase (GST), cytochrome CYP1A1 and CYP2E1 polymorphisms and lung cancer susceptibility. Methods A case-control study was conducted in 91 patients with newly diagnosed primary lung cancer in Guangdong and 91 inpatients with non-pulmonary disorders in the same period. Polymerase chain reaction (PCR) and restriction fragment length polymorphism RFLP) technique was used to detect CYP1A1, CYP2E1 and GSTM1 gene polymorphisms in patients and controls. Results The OR of CYP1A1 mutant (m2m2) was 1.51 compared with that of wild type (mlml). The OR of CYP2E1C1C1 and C1C2 was 1.80. The OR of C2C2 and C1C2 was 5.48. The deletion of GSTM1 was compared with that of normal. OR 1.26. The combined analysis of the two genes showed that OR of GSTM1 gene was 2.29 compared with that of GSTM1 gene and CYP1A1m1m1 gene. The OR of GSTM1 gene with CYP2E1C1C1 and CYP2E1C1C1 was 2.13 Compared with those carrying CYP1A1m2m2 and CYP2E1C1C1 and those carrying CYP1A1m1m1 and CYPE1c1c2, the odds ratio (OR) of 3.00.3 genes showed that patients carrying CYP1A1m2m2 and CYP2E1C1C1 with GSTM1 gene deletion had higher CYP1A1m1m1 and CYP2E1c1c2 The normal GSTM1 gene increased the risk of lung cancer, OR 3.97. Conclusions CYP1A1, CYP2E1 and GSTM1 showed no relationship with the risk of lung cancer in the univariate analysis. The combined effect of the two genes and the three genes seemed to increase the risk of lung cancer, but not statistically significant. These three genes suggest that these three genes are not the main effect of individual susceptibility to lung cancer genes, may be secondary genes.