文章摘要
龙喜带,马韵,韦义萍,邓卓霖.广西地区人群gstM1和gstT1编码基因型多态性与肝细胞癌易感性分析[J].中华流行病学杂志,2005,26(10):777-781
广西地区人群gstM1和gstT1编码基因型多态性与肝细胞癌易感性分析
Study on the detoxication gene gstM1-.gstT1-null and susceptibility to aflatoxin B1-related hepatocellular carcinoma in Guangxi
收稿日期:2004-11-11  出版日期:2014-09-15
DOI:
中文关键词: 肝细胞肿瘤;空白基因型;黄曲霉毒素B1
英文关键词: Hepatocellular neoplasms;Null genotype;Aflatoxin B1
基金项目:国家自然科学基金资助项目(39860032);广西壮族自治区教育厅重点资助项目(98-2-8)
作者单位E-mail
龙喜带 530021 南宁, 广西医科大学病理学教研室  
马韵 530021 南宁, 广西医科大学病理学教研室 yunandama@hotmail.com.cn 
韦义萍 530021 南宁, 广西医科大学病理学教研室  
邓卓霖 广西医科大学护理学院病理学教研室  
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中文摘要:
      目的 探讨解毒酶基因gstM1和gstT1的空白基因型(null)与黄曲霉毒素B1(AFB1) 相关肝细胞癌(HCC)的易感性。方法 应用聚合酶链反应技术对广西地区AFB1高污染区140例HCC患者和536例对照人群的gstM1和gstT1基因多态性进行检测,进行以医院为基础的病例对照研究。结果gstM1-present基因型和gstT1-present基因型为HCC保护基因型,而二者的null基因型为HCC风险基因型,其校正OR值(95%CI)分别为2.07(1.20~3.57)和1.44(0.85~2.45);②在同时有gstM1和gstT1两个基因缺失的个体中其患癌风险比单一缺失者大(校正OR=2.43,95%CI:1.19~4.97);③gstM1-和gstT1-null基因型与AFB1暴露程度在HCC发病中具有协同作用,从中低度至高度AFBsub>1暴露时,其校正OR值(95%CI)分别升高达12.76(5.38~30.24)和7.82(3.61~ 16.90)。结论 解毒酶基因gstM1和gstT1多态性与HCC易感性相关,二者的null基因型均增加患HCC风险,二者同时出现时患HCC风险更为明显;gstM1和gstT1的null基因型在HCC发病中与AFB1暴露程度呈正相关。
英文摘要:
      Objective To study the association between susceptibility to aflatoxin B1(AFB1)-related hepatocellular carcinoma(HCC) and the null genotypes of detoxication gene gstM1 and gstT1. Methods Peripheral blood white blood cells DNA samples were obtained from all the subjects including 140 HCC cases and 536 controls from AFB1 high risk area Guangxi. gstM1 and gstT1 polymorphisms were detected by polymerase chain reaction technique. Results (1)gstM1- and gstT1-present were associated with decreasing risk of HCC. gstM1- and gstT1-null were associated with the increasing risk of Hcc [adjusted OR(95%CI)=2.07(1.20~3.57) and 1.44(0.85~2.45), respectively]; (2) The appearance of both gstM1- and gstT1-null genotypes were more susceptible to HCC than either one of them (adjusted OR and 95%CI are 2.43 and (1.19~4.97);(3)From low/median to high level of AFB1 exposure, both gstM1- and gstT1-null genotypes were associated with significantly conspicuous increasing risk of HCC [adjusted OR (95%CI)=12.76(5.38~30.24) and 7.82(3.61~ 16.90) respectively]. Conclusion It was suggested that: genetic polymorphisms of gstM1 and gstT1 were susceptible to HCC; individuals who were gstM1- or gstT1-null would have an increasing risk of developing HCC while individuals with both nulls were more susceptible. There was evidence of interaction between gstM1- and gstT1-null and the level of gstM1 exposure which was associated with the increasing risk of HCC.
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