Abstract
陈道俊,丁锐,曹炜,叶冬青.NQO1C609T、XRCC1G28152A基因多态性与吸烟的交互作用和胃癌的关系[J].Chinese journal of Epidemiology,2011,32(1):5-8
NQO1C609T、XRCC1G28152A基因多态性与吸烟的交互作用和胃癌的关系
Interaction between polymorphisms in NQO1C609T and XRCC1G28152A and their correlation with smoking on gastric cancer
Received:September 09, 2010  
DOI:
KeyWord: 胃肿瘤  NQO1基因  XRCC1基因  吸烟
English Key Word: Gastric neoplasms  NAD (P)H quinone oxidoreductase 1  X-ray repair cross complementing group 1  Smoking
FundProject:安徽省教育厅青年教师项目(2008jql064)
Author NameAffiliationE-mail
CHEN Dao-jun   
DING Rui   
CAO Wei   
YE Dong-qing  cjdcp@mail.hf.ah.cn 
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Abstract:
      目的 探讨NQO1C609T、XRCC1G28152A基因多态性与吸烟的交互作用和胃癌的关系。方法 采用1:1配对病例对照研究方法,应用PCR-RFLP对基因多态性进行分析,根据交互系数γ判断交互作用类型,探询胃癌可能的遗传及环境因素。结果 334例胃癌患者,平均年龄在57岁,其中男性占65.3%;病例组吸烟率(55.09%)显著高于对照组(36.53%);NQO1C609T基因杂合突变型(CT)、纯合突变型(TT)增加了胃癌的发病风险(OR值分别为1.507、3.050);XRCC1G28152A基因多态性与胃癌遗传易感性没有关系;同时携带XRCC1AG和NQO1TT个体较XRCC1AG和NQO1CC个体胃癌的发病增加2.789倍;携带XRCC1GG和NQO1TT个体的胃癌发病风险是XRCC1GG和NQO1CC个体的4.448倍;NQO1纯合突变型(TT)与吸烟在胃癌发生中有正向交互作用(OR=4.057,γ=1.272),XRCC1纯合突变型(GG)与吸烟在胃癌发生中有正向交互作用(OR=3.094,γ=2.070)。结论 NQO1、XRCC1基因多态性与吸烟的交互作用增加了胃癌发病风险。胃癌的发生表现为基因及环境因素综合作用的结果。
English Abstract:
      Objective To investigate the relationship between polymorphism of NAD (P) H quinone oxidoreductase 1 (NQO1) and X-ray repair cross-complementing group 1 (XRCC1) and their correlation with smoking on the susceptibility to gastric cancer. Methods A 1: 1 case-control study of 334 patients with primary gastric cancer, with non-cancer or alimentary inpatients as control group (matched for ages ± 5 years, sex and reqion) in Anhui province was conducted to analyze theNQO1C609T and XRCC1G28152A. Gene types by PCR-based restriction fragment length polymorphism techniques. Interaction index (γ) was calculated to determine the type of gene-environment interaction. Results The average age of 334 cases of gastric cancer patients was 57 years, with 65.3% of them were male. Smoking rate in the case group (55.09%) was significantly higher than in the control group (36.53%). The consequence showing that it carried the heterozygous variant (CT) or homozygous variant (TT) of NQO1 could enhance the risk of gastric cancer (OR=1.507, 3.050), but not the XRCC1G28152A gene polymorphism or the susceptibility to gastric cancer. At the same time, individuals that carrying XRCC1AG and NQO1TT could increase 2.789 times the incidence of gastric cancer than those who carrying the XRCC1AG or NQO1CC. The gastric cancer risk of XRCC1GG individuals that carrying NQO1TT was 4.448 times higher than those who carrying XRCC1GG or NQO1 CC. The positive interactions of NQO1 homozygous variant (TT), XRCC1 homozygous variant (GG) and smoking were revealed in the occurrence rates of gastric cancer (OR=3.094, γ=2.070). Conclusion Our research findings showed that the significant interactions between genetic polymorphisms of NQO1, XRCC1 and smoking added the risk of gastric cancer, while genetic and environmental hazardous factors co-effecting the development of gastric cancer.
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