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山东胃癌高低发人群Lewis基因多态性分析 被引量:1

Analysis of Lewis Gene Polymorphism in High and Low Incidence Area of Gastric Cancer in Shandong Province
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摘要 应用PCR产物直接测序的方法,检测山东省胃癌高发的临朐人群和低发的苍山人群中Lewis基因多态性T59G的分布,旨在探讨山东临朐和苍山地区胃癌发病率显著不同的内在原因,为阐明临朐地区胃癌高发的机制提供实验依据。结果表明,T59G突变个体在临朐和苍山人群中的分布频率分别为34.5%和31.6%,差别无统计学意义,P>0.05,OR为1.14(95%CI,0.59~2.19)。提示就此点突变而言,临朐人群和苍山人群为同一人群,具有极其相似的遗传背景;T59G不能作为区分临朐和苍山人群的遗传标志,与这两个地区胃癌发病的区别没有相关性。 To explore the cause leading to the difference in incidence of gastric cancer between Linqu and Cangshan populations,Shandong Province,and to provide evidence for the possible mechanism of high incidence of gastric cancer in Linqu County,the distribution of T59G mutation in Lewis gene was screened between Linqu and Cangshan populations by PCR-sequencing.The frequency of individuals with T59G mutation was 34.5% in Linqu population and 31.6% in Cangshan population,respectively,with no significant difference,P>0.05,and OR is 1.14 (95% CI,0.59~2.19).This suggests that Linqu and Cangshan populations may share the same genetic background.T59G mutation of Lewis gene could not be used as a genetic marker for Linqu and Cangshan populations and is not relevant to the difference in incidence of gastric cancer between them.
出处 《遗传》 CAS CSCD 北大核心 2003年第3期258-260,共3页 Hereditas(Beijing)
基金 国家973重大项目基金(1998051203)资助~~
关键词 山东 胃癌 高发人群 低发人群 Lewis基因 多态性 T59G gastric cancer high and low incidence populations Lewis gene polymorphism
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参考文献8

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二级参考文献16

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共引文献7

同被引文献15

  • 1李连弟,鲁凤珠,张思维,牧人,孙秀娣,皇甫小梅,孙杰,周有尚,欧阳宁慧,饶克勤,陈育德,孙爱明,薛志福,夏毅.中国恶性肿瘤死亡率20年变化趋势和近期预测分析[J].中华肿瘤杂志,1997,19(1):3-9. 被引量:869
  • 2Wei-cheng You, Lian Zhang, Mitchell H. Gail, et al. Gastric dysplasia and gastric cancer: Helicobacter pylori, Serum Vitamin C,and other risk factors [J]. J Natl Cancer Inst,2000,92:1607~1612.
  • 3Kuipers E J. Helicobacter pylori and the risk and management of associated diseases: gastritis, ulcer disease, atrophic gastritis and gastric cancer [J]. Aliment Phamacol Ther, 1997,11 (suppl. 1) :71~88.
  • 4Correa P. Helicobacter pylori and gastric carcinogenesis [J].Am J Surg Pathol,1995,19(suppl 1) :s37~43.
  • 5Fontham E T H,Ruiz B,Perez A,et al. Determinants of helicobacter pylori infection and chronic gastritis [J]. Am J Gastroenterol, 1995,90: 1094~ 100.
  • 6Holcombe C. Helicobacter pylori; the African Enigma [J].Gut,1992,33:429~431.
  • 7Azuma T,Ito Y,Miyaji H,et al. Immunogenetic analysis of the human leukocyte antigen DQA1 lotusin patients with duodenal ulcer or chronic atrophic gastritis harbouring Helicobacter pylori[J]. Eur J Gastroent Hepat,1995,7:s71~73.
  • 8Emad M, EI-Omar, Mary Carrington,et al. Interleukin-1 polymorphisms associated with increased risk of gastric cancer [J].Nature, 2000,404: 398 ~402.
  • 9Simoons-Smit I M,Appelmelk A J,Theo Verboom,et al. Typing of Helicobacter pylori with monoclonal antibodies against lewis antigens in Lipopolysaccharide [J]. JCM, 1996,34 (g):2196~2200.
  • 10Ge Wang, Zhongming Ge, David A. Rasko, et al. Lewis antigens in Helicobacter pylori:biosynthesis and phase variation[J]. Mol Micro,2000,36(6) :1187~1196.

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