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DNA修复基因XRCC3多态性与肺癌易感性的关系

[Relationship between polymorphisms of DNA repair gene XRCC3 and susceptibility to lung cancer].

作者信息

Zhang Zeng-Li, Zhou Cai-Cun, Zhang Jie, Tang Liang, Su Bo

机构信息

Laboratory of Lung Cancer, Shanghai Pulmonary Hospital, Shanghai, China.

出版信息

Zhonghua Jie He He Hu Xi Za Zhi. 2007 Dec;30(12):936-40.

Abstract

OBJECTIVE

To study the polymorphisms of DNA repair gene XRCC3 and the relationship between genetic variations and susceptibility to lung cancer.

METHODS

A case-control study of 291 patients with lung cancer and 273 cancer-free subjects as a control group was conducted from September 2006 to January 2007 to detect XRCC3 polymorphisms at loci. Genotypes of XRCC3 were analyzed by real time PCR using Taqman probes.

RESULTS

Compared with never smoking subjects with wild homozygous genotype (Thr/Thr), smokers with the same genotytpe (Thr/Thr) had increased risk of lung cancer, adjusted odds ratio (OR) was 2.467 (95% CI: 1.49 - 4.08, P < 0.001). Smokers with the heterozygous genotype (Thr/Met) also had increased risk of lung cancer, adjusted OR was 2.283 (95% CI: 1.21 - 6.60, P < 0.05). XRCC3 codon 241 homozygous genotype (Thr/Thr) and pack-years of smoking less than 30 had a weak protective effect on adenocarcinoma (OR = 0.49, 95% CI: 0.26 - 0.93, P < 0.05). Allel Met of XRCC3 codon 241 and smoking conferred an increased risk of squamous cell carcinoma (OR = 9.69, 95% CI: 3.27 - 28.72, P < 0.01). Those with allel Met of XRCC3 codon 241 and pack-years of smoking less than 30 or more than 30 had different risk of squamous cell carcinoma, the OR was 8.00 (95% CI: 1.97 - 32.52, P < 0.01), and 11.67 (95% CI: 2.98 - 45.73, P < 0.01) respectively.

CONCLUSION

The results demonstrated that genetic polymorphism of XRCC3 DNA repair gene may contribute to the susceptibility to lung cancer and have synergistic effect with smoking.

摘要

目的

研究DNA修复基因XRCC3的多态性以及基因变异与肺癌易感性之间的关系。

方法

于2006年9月至2007年1月进行了一项病例对照研究,以291例肺癌患者为病例组,273例无癌受试者为对照组,检测位点处的XRCC3多态性。采用Taqman探针通过实时PCR分析XRCC3的基因型。

结果

与野生纯合基因型(Thr/Thr)的从不吸烟受试者相比,具有相同基因型(Thr/Thr)的吸烟者患肺癌的风险增加,调整后的优势比(OR)为2.467(95%CI:1.49 - 4.08,P < 0.001)。具有杂合基因型(Thr/Met)的吸烟者患肺癌的风险也增加,调整后的OR为2.283(95%CI:1.21 - 6.60,P < 0.05)。XRCC3密码子241纯合基因型(Thr/Thr)且吸烟包年数少于30对腺癌有较弱的保护作用(OR = 0.49,95%CI:0.26 - 0.93,P < 0.05)。XRCC3密码子241的Met等位基因与吸烟会增加鳞状细胞癌的风险(OR = 9.69,95%CI:3.27 - 28.72,P < 0.01)。具有XRCC3密码子241的Met等位基因且吸烟包年数少于30或多于30的人患鳞状细胞癌的风险不同,OR分别为8.00(95%CI:1.97 - 32.52,P < 0.01)和11.67(95%CI:2.98 - 45.73,P < 0.01)。

结论

结果表明,XRCC3 DNA修复基因的遗传多态性可能与肺癌易感性有关,并与吸烟具有协同作用。

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