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目的:评估若干遗传学因素与一个环境因素对患前列腺癌风险的联合调节作用。本文重点关注与细胞调控有关的低外显基因的等位变体、解毒过程和吸烟这几个因素。方法:本研究设了病例对照。研究分析了携 p53cd72 Pro 等位基因、CYP1A1 M1等位基因和 GSTM1 null 基因型的人群与他们患前列腺癌的风险之间的关联。结果:携 Pro~*和 M1~*,Pro~*和 GSTM1null 或 GSTM1 null 和 CYP1A1 M1~*等位变体的吸烟者的联合患病风险显著高于对照组(优势比[odds ratio:OR]:13.13,95%置信区间[CI]:2.41-71.36;OR:3.97,95% CI:1.13-13.95;OR:6.87,95% CI:1.68-27.97),非吸烟组的患病风险与对照组相比无显著差异。与非吸烟者和无患病风险组相比,p53cd72,GSTM1和 CYP1A1 M1在吸烟者中的组合极明显地与前列腺癌患病风险有关联(OR:8.87,95% CI:1.25-62.71)。结论:本文实验结果表明,在研究人群中,p53cd72,CYP1A1和GSTM1等位基因与吸烟因素的组合对前列腺癌患病风险的改变起重要作用,这意味着携敏感基因型的吸烟者可能比携带非敏感基因型的吸烟者患前列腺癌的风险更大。
PURPOSE: To assess the combined effect of several genetic factors and one environmental factor on the risk of developing prostate cancer. This article focuses on the alleles of the low-allele associated with cellular regulation, the detoxification process, and smoking. Methods: This study set up a case-control. The association between the population carrying the p53cd72 Pro allele, the CYP1A1 M1 allele and the GSTM1 null genotype and their risk of developing prostate cancer was analyzed. Results: The combined risk of smokers with Pro ~ * and M1 ~ *, Pro ~ * and GSTM1null or GSTM1 null and CYP1A1 M1 ~ * alleles was significantly higher than that of the control group (odds ratio: OR) : 13.13, 95% confidence interval [CI]: 2.41-71.36; OR: 3.97, 95% CI: 1.13-13.95; OR: 6.87, 95% CI: 1.68-27.97) No significant difference compared to. The combination of p53cd72, GSTM1 and CYP1A1 M1 in smokers was most significantly associated with the risk of prostate cancer (OR: 8.87, 95% CI: 1.25-62.71) compared to nonsmokers and the no-risk group. CONCLUSIONS: Our results demonstrate that the combination of the p53cd72, CYP1A1, and GSTM1 alleles and smoking factors in study populations play an important role in the risk of prostate cancer, suggesting that smokers with sensitive genotypes may be more likely to carry Smokers with non-sensitive genotypes have a greater risk of prostate cancer.