Association of MUTYH Gln324His and APEX1 Asp148Glu with colorectal cancer and smoking in a Japanese population.
Association of MUTYH Gln324His and APEX1 Asp148Glu with colorectal cancer and smoking in a Japanese population.
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DOI：
10.1186/1756-9966-27-49
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发表时间：
2008-09-30
期刊：
影响因子：
--
通讯作者：
Takahashi J
中科院分区：
文献类型：
--
作者：
Kasahara M;Osawa K;Yoshida K;Miyaishi A;Osawa Y;Inoue N;Tsutou A;Tabuchi Y;Tanaka K;Yamamoto M;Shimada E;Takahashi J
DNA修复酶基因多态性可能导致遗传不稳定和结直肠癌的发生。我们的目的是测量结直肠癌中修复基因多态性和吸烟之间的相互作用。病例对照研究包括68例结直肠癌患者和121例非癌症对照，根据吸烟包年数分为非吸烟者和吸烟者。采用PCR-RFLP方法检测DNA修复酶基因OGG 1 Ser 326 Cys、MUTYH Gln 324 His、APEX 1 Asp 148 Glu和XRCC 1 Arg 399 Gln的遗传多态性。MUTYH Gln 324 His显示与结直肠癌风险有很强的显著相关性（粗比值比[OR] 3.30，95%置信区间[95%CI] 1.44-7.60，p = 0.005;校正OR 3.53，95%CI 1.44-8.70，p = 0.006）。APEX 1 Asp 148 Glu的OR具有统计学显著性（粗OR 2.69，95%CI 1.45-4.99，p = 0.002;校正OR 2.33，95%CI 1.21-4.48，p = 0.011）。对于结肠癌，MUTYH Gln 324 His和APEX 1 Asp 148 Glu的OR具有统计学显著性（MUTYH Gln 324 His的校正OR 3.95，95%CI 1.28-12.20，p = 0.017; APEX 1 Asp 148 Glu的校正OR 3.04，95%CI 1.38-6.71，p = 0.006）。烟草暴露和MUTYH Gln 324 His的联合作用显示与非吸烟者的结直肠癌风险显著相关（校正OR 4.08，95%CI 1.22-13.58，p = 0.022），吸烟者的APEX 1 Asp 148 Glu显著增加（校正OR 5.02，95%CI 1.80-13.99，p = 0.002）。然而，OGG 1 Ser 326 Cys和XRCC 1 Arg 399 Gln的分布与结直肠癌风险无关。我们的研究结果表明，MUTYH Gln 324 His和APEX 1 Asp 148 Glu构成了结直肠癌，特别是结肠癌的风险增加。MUTYH Gln 324 His与从不吸烟史的结直肠癌易感性密切相关，而APEX 1 Asp 148 Glu基因型在伴随吸烟暴露时构成结直肠癌风险增加。
Genetic polymorphisms of DNA repair enzymes may lead to genetic instability and colorectal cancer carcinogenesis. Our objective was to measure the interactions between polymorphisms of repair genes and tobacco smoking in colorectal cancer. The case-control study involved sixty-eight colorectal cancer patients and 121 non-cancer controls divided into non-smokers and smokers according to pack-years of smoking. The genetic polymorphisms of DNA repair enzymes,OGG1 Ser326Cys, MUTYH Gln324His, APEX1 Asp148Glu and XRCC1 Arg399Gln, were examined using PCR-RFLP. The MUTYH Gln324His showed strong significant associations with a risk of colorectal cancer (crude odds ratio [OR] 3.30, 95% confidence interval [95%CI] 1.44–7.60, p = 0.005; adjusted OR3.53, 95%CI 1.44–8.70, p = 0.006). The ORs for the APEX1 Asp148Glu were statistically significant (crude OR 2.69, 95%CI 1.45–4.99, p = 0.002; adjusted OR 2.33, 95%CI 1.21–4.48, p = 0.011). The ORs for the MUTYH Gln324His and the APEX1 Asp148Glu were statistically significant for colon cancer (adjusted OR 3.95, 95%CI 1.28–12.20, p = 0.017 for MUTYH Gln324His ; adjusted OR 3.04, 95%CI 1.38–6.71, p = 0.006 for APEX1 Asp148Glu). The joint effect of tobacco exposure and the MUTYH Gln324His showed a significant association with colorectal cancer risk in non-smokers (adjusted OR 4.08, 95%CI 1.22–13.58, p = 0.022) and the APEX1 Asp148Glu was significantly increased in smokers (adjusted OR 5.02, 95%CI 1.80–13.99, p = 0.002). However, the distributions of OGG1 Ser326Cys and XRCC1 Arg399Gln were not associated with a colorectal cancer risk. Our findings suggest that the MUTYH Gln324His and the APEX1 Asp148Glu constitutes an increased risk of colorectal cancer, especially colon cancer. The MUTYH Gln324His is strongly associated with colorectal cancer susceptibility in never smoking history, whereas the APEX1 Asp148Glu genotype constitutes an increased risk of colorectal cancer when accompanied by smoking exposure.
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影响因子：
14.9
作者：
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