论文部分内容阅读
目的研究 DNA 修复基因 XRCC3多态性与肺癌易感性的关系。方法采用病例-对照研究,于2006年9月至2007年1月收集上海肺科医院原发性肺癌患者291例及同期住院的非肿瘤患者273例,应用 Taqman 探针结合实时荧光 PCR 方法分析病例组和对照组 XRCC3基因Thr241Met 的多态性分布,比较不同基因型与肺癌易感性的关系以及基因多态性与吸烟对肺癌的交互作用。对照组与病例组的比较用 X~2检验,以调整比值比及95%可信区间表示相对危险度,所有统计检验均为双侧概率检验,所有资料均用 SPSS 软件进行统计。结果与携带 XRCC3密码子241野生纯合基因型(Thr/Thr)且不吸烟者相比,携带同样基因型且吸烟者患肺癌的风险会增加,其调整比值比(OR 值)为2.47[95%可信区间(CI)为1.49~4.08,P<0.01];携带有杂合基因型(Thr/Met)且吸烟者患肺癌的风险也会增加,其调整 OR 值为2.28(95%CI 为1.21~6.60,P=0.017)。野生纯合基因型(Thr/Thr)且吸烟量少于30包年可能对肺腺癌有较弱的保护作用(OR=0.49,95%CI 为0.26~0.93,P=0.03)。携带有 XRCC3密码子241Met 等位基因且吸烟者患肺鳞癌的风险明显增加(调整 OR=9.69,95%CI 为3.27~28.72,P<0.01)。携带241Met 等位基因且吸烟剂量<30包年和≥30包年的患者患肺鳞癌的风险也不同,OR 值分别为8.00(95%CI 为1.97~32.52,P<0.01)和11.67(95%CI 为2.98~45.73,P<0.01)。结论 DNA 修复基因 XRCC3多态性可能对肺癌易感性产生影响,并可能与吸烟有一定的协同作用。
Objective To study the relationship between DNA repair gene XRCC3 polymorphism and lung cancer susceptibility. Methods A case-control study was conducted. From September 2006 to January 2007, 291 cases of primary lung cancer and 273 non-tumor patients were enrolled in Shanghai Pulmonary Hospital. The patients were analyzed by Taqman probe combined with real-time fluorescence PCR Group and control group XRCC3 Thr241Met polymorphism distribution, comparison of different genotypes and lung cancer susceptibility and genetic polymorphisms and smoking on lung cancer interaction. The control group and the case group were compared with X ~ 2 test to adjust the odds ratio and the 95% confidence interval to represent the relative risk. All statistical tests were double-sided probability test, and all the data were calculated by SPSS software. Results Compared with non-smokers carrying XRCC3 codon 241 wild-type homozygote (Thr / Thr), smokers with the same genotype had an increased risk of developing lung cancer with a adjusted odds ratio (OR) of 2.47 [95 % Confidence interval (CI) ranged from 1.49 to 4.08, P <0.01]. The risk of lung cancer in smokers with heterozygous genotypes (Thr / Met) also increased with a adjusted OR of 2.28 (95% CI 1.21 ~ 6.60, P = 0.017). Wild homozygous genotypes (Thr / Thr) and smoking less than 30 years may have a weaker protective effect on lung adenocarcinoma (OR = 0.49, 95% CI 0.26-0.93, P = 0.03). The risk of lung squamous cell carcinoma with XRCC3 codon 241Met allele was significantly increased (adjusted OR = 9.69, 95% CI 3.27-28.72, P <0.01). Patients with the 241Met allele who smoked at <30 years and ≥30 years had different risk of squamous cell lung cancer with odds ratios of 8.00 (95% CI 1.97 to 32.52, P <0.01) and 11.67 (95) % CI was 2.98 ~ 45.73, P <0.01). Conclusion DNA repair gene XRCC3 polymorphism may have an impact on susceptibility to lung cancer and may have some synergistic effects with smoking.