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CYP2E1 and GSTM1 gene polymorphisms, environmental factors, and the susceptibility to lung cancer

机译:CYP2E1和GSTM1基因多态性,环境因素和肺癌易感性

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Objective To investigate the relationships between the CYP2E1 RsaI polymorphism, GSTM1 polymorphism, and the susceptibility to lung cancer, along with the interactions between environmental factors and these genes. Methods A case‐control study was carried out to explore the independent effect of gene polymorphisms on risk of lung cancer, and the combined effects of gene loci. The stratification analysis of age, sex, smoking, and drinking combined with positive loci was also analyzed, and any interaction was identified. Results The logistic regression analysis showed that there were statistical relationships between the CYP2E1 RsaI TT genotype and lung cancer, GSTM1 (?) and lung cancer. The combined effect's analysis of these 2 loci showed that, with an increase in the number of risk alleles, the risk of lung cancer also increased (supposing 0 risk allele as the reference group). Subjects carrying 3 risk alleles had the highest risk of developing lung cancer with an adjusted OR?=?10.38 (95% CI 2.10‐51.35). Stratified analysis showed that, in women, nonsmoking subjects, or nondrinking subjects, the combined effects could increase the risk of lung cancer; no heterogeneity was found between these layers except sex. The interaction analysis showed that, supposing the male, GSTM1 (+) genotype as the reference, the female, GSTM1 (?) genotype had a significantly increased risk of lung cancer (OR?=?2.17 [1.01‐4.70]); when the non‐smoking, GSTM1 (+) genotype subjects was the reference group, smoking, GSTM1 (+) genotype subjects and smoking, GSTM1 (‐) genotype subjects had significantly higher risk of lung cancer (OR?=?2.00 [1.01‐3.96], OR?=?2.89 [1.28‐6.54]). Conclusion CYP2E1 RsaI TT genotype was a protective factor against the development of lung cancer, while GSTM1 (?) genotype was a risk factor for lung cancer. Increases in the number of the risk alleles also increased lung cancer risk. GSTM1 (?) genotype, sex, and smoking status might interact in the incidence of lung cancer.
机译:目的探讨CYP2E1基因RsaI基因多态性,GSTM1基因多态性与肺癌易感性的关系,以及环境因素与这些基因的相互作用。方法进行病例对照研究,探讨基因多态性对肺癌风险的独立影响以及基因位点的综合影响。还分析了年龄,性别,吸烟和饮酒与阳性基因座的分层分析,并确定了任何相互作用。结果Logistic回归分析表明CYP2E1 RsaI TT基因型与肺癌,GSTM1(?)和肺癌之间存在统计学关系。对这2个基因座的综合效应分析表明,随着风险等位基因数量的增加,肺癌的风险也增加了(假设0个风险等位基因为参考组)。携带3个风险等位基因的受试者患肺癌的风险最高,OR == 10.38(95%CI 2.10-51.35)。分层分析显示,在女性,非吸烟对象或非饮酒对象中,综合作用可能增加患肺癌的风险;除性别外,在这些层之间未发现异质性。相互作用分析表明,假设男性为GSTM1(+)基因型,女性为GSTM1(?)基因型,则患肺癌的风险显着增加(OR == 2.17 [1.01-4.70])。当非吸烟GSTM1(+)基因型受试者为参照组时,吸烟,GSTM1(+)基因型受试者和吸烟GSTM1(‐)基因型受试者患肺癌的风险显着更高(OR?=?2.00 [1.01- 3.96],或?=?2.89 [1.28-6.54])。结论CYP2E1 RsaI TT基因型是肺癌发生的保护因素,而GSTM1(?)基因型是肺癌的危险因素。风险等位基因数量的增加也增加了肺癌的风险。 GSTM1(?)基因型,性别和吸烟状况可能与肺癌的发生有关。

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