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脆性组氨酸三联体基因转录外显子丢失与肝细胞癌易感性的Meta分析
引用本文:张成,柯阳,吴雪松,施智甜,谭宇棋,王维,黎建福,王琳.脆性组氨酸三联体基因转录外显子丢失与肝细胞癌易感性的Meta分析[J].肿瘤防治研究,2015,42(11):1124-1127.
作者姓名:张成  柯阳  吴雪松  施智甜  谭宇棋  王维  黎建福  王琳
作者单位:650101昆明,昆明医科大学第二附属医院肝胆外科
基金项目:国家自然科学基金(81060204,81360360);云南省卫生厅卫生系统学科带头人培养计划项目(D-201220)
摘    要:目的 探讨脆性组氨酸三联体(Fhit)基因外显子丢失与肝细胞癌(HCC)发病风险的关系。方法 检索PubMed、CNKI、万方等数据库,收集有关Fhit基因转录外显子丢失与HCC易感性的病例对照研究,并从纳入文献中提取数据进行Meta分析。结果 最终纳入7个研究,涉及肝炎病毒相关HCC162例,对照组170例包括癌旁肝硬化组织136例,正常肝组织34例。HCC组与对照组Fhit外显子丢失比较的OR=5.02(95%CI: 2.99~8.43,P<0.00001);亚组分析显示,HCC组与癌旁肝硬化组织组比较的OR=3.55(95%CI: 2.06~6.13,P<0.00001);癌旁肝硬化组织组与正常肝组织组比较的OR=8.23(95%CI: 1.47~45.94,P=0.02)。结论 Fhit基因转录过程中外显子丢失可能是HCC发生的危险因素;肝炎病毒可能作用于肝细胞Fhit基因脆性位点造成其转录过程中外显子丢失,引起肝细胞恶变。

关 键 词:Fhit基因  肝细胞癌  转录  外显子  系统评价  Meta分析  
收稿时间:2014-11-10

Relationship Between Fragile Histidine Trial Gene Exon Loss and Susceptibility of Hepatocellular Carcinoma: A Meta-analysis
ZHANG Cheng,KE Yang,WU Xuesong,SHI Zhitian,TAN Yuqi,WANG Wei,LI Jianfu,WANG Lin.Relationship Between Fragile Histidine Trial Gene Exon Loss and Susceptibility of Hepatocellular Carcinoma: A Meta-analysis[J].Cancer Research on Prevention and Treatment,2015,42(11):1124-1127.
Authors:ZHANG Cheng  KE Yang  WU Xuesong  SHI Zhitian  TAN Yuqi  WANG Wei  LI Jianfu  WANG Lin
Institution:Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming 650101, China
Abstract:Objective To investigate the relationship between Fhit gene exon loss and risk of hepatocellular carcinoma(HCC). Methods By searching PubMed, CNKI, Wanfang Database, et al, the case-control studies about the relationship between Fhit gene exon loss and the risk of HCC were chosen. Then the Meta-analysis was conducted using odd rate(OR) and 95% confidential interval(CI) to assess the strength of association. Results Seven studies were finally chosen, including 162 hepatitis virus-related HCC cases and 170 controls(136 tumor-adjacent cirrhosis and 34 normal liver tissues). The risk of Fhit gene exon loss was higher in the HCC group than that in the control group(OR=5.02, 95%CI: 2.99-8.43, P<0.00001). Subgroup analysis showed the risk of Fhit gene exon loss was higher in HCC tissues than that in tumor-adjacent cirrhosis tissues(OR=3.55, 95%CI: 2.06-6.13, P<0.00001); and it was also higher in tumor-adjacent cirrhosis tissues than that in normal liver tissues(OR=8.23, 95%CI: 1.47-45.94, P=0.02). Conclusion Fhit gene exon loss may be notably correlated with hepatocellular carcinoma, and HBV or HCV may play a role in the development of HCC through leading the Fhit gene exon loss.
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