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食管癌与幽门螺杆菌L型感染和PCNA、CerbB-2、P53表达的关系
引用本文:于东红,贾继辉,李新芝,王萍,唐素兰,姚敏. 食管癌与幽门螺杆菌L型感染和PCNA、CerbB-2、P53表达的关系[J]. 中国人兽共患病杂志, 2002, 18(5): 16-18,F004
作者姓名:于东红  贾继辉  李新芝  王萍  唐素兰  姚敏
作者单位:蚌埠医学院病理学教研室 蚌埠(于东红),山东医科大学微生物教研室 233003(贾继辉),临泉县人民医院 蚌埠(李新芝),蚌埠医学院病理学教研室 233003(王萍),蚌埠医学院微生物教研室 蚌埠(唐素兰),蚌埠医学院病理学教研室 233003(姚敏)
基金项目:安徽省教育厅科研基金资助项目 (No 2 0 00JL163 )
摘    要:
目的 探讨幽门螺杆菌L型 (Hp -L)感染和PCNA、CerbB - 2、P53 表达在食管癌发生机制中的作用。方法 应用免疫组化和革兰染色技术检测 112例食管癌和 30例对照组的Hp -L型、PCNA、CerbB - 2、和P53 基因蛋白 ,对Hp -L型阳性和阴性组织的PCNA、CerbB - 2和P53 表达进行比较分析。结果 癌组的革兰染色L型检出率 (6 7 9% )与对照组 (2 6 7% )有显著性差异 (P <0 0 5 ) ;与免疫组化Hp -L型抗原表达阳性率 (6 5 2 % )无显著性差异 (P >0 0 5 ) ,Hp -L型检出阳性率为6 1 6 % (6 9/ 112 )。癌组的PCNA、CerbB - 2、P53 表达阳性率明显高于对照组 ,癌组中Hp -L型感染阳性组的PCNA、CerbB -2、P53 表达阳性率也高于其Hp -L型阴性组 ,其差异均有显著性 (P <0 0 5 )。表明Hp -L型感染与食管癌相关 ,与食管癌的PCNA、CerbB - 2、P53 过表达也相关。结论 Hp -L型有可能通过促使细胞增殖加速和致基因突变而涉及食管癌的发生过程

关 键 词:食管肿瘤  幽门螺杆菌  L型  增殖细胞核抗原  癌基因
文章编号:1002-2694(2002)05-0016-03

Helicobacter Pylori L-form Infection and Expression of PCNA,CerbB-2,p53 in Esophageal Cancer
YU Donghong,JIA Jihui,LI Xinzhi et al. Helicobacter Pylori L-form Infection and Expression of PCNA,CerbB-2,p53 in Esophageal Cancer[J]. Chinese Journal of Zoonoses, 2002, 18(5): 16-18,F004
Authors:YU Donghong  JIA Jihui  LI Xinzhi et al
Abstract:
Aim To investigate the impact of Helicobacter Pylori L form(Hp L)and the PCNA,CerbB 2 and P 53 on the carcinogenesis of esophageal cancer(EC) Methods Gram stain and immunohistochemical techniques were used to detect the Hp L infection and the expression of PCNA protein and CerbB 2,P 53 oncoproteins in 112 tissues of esophageal squamous cell cancer and 30 normal tissues of esophageal squamous epithelials Results The positive rate of the infection of bacterial L form(67 9%)in cancer group was significantly higher than that in normal group(26 7%)with Gram stain(P<0 05) The antigen of Hp L in 65 2% cases was detected by immunohistochemical techniques There was no difference between the results obtained from each staining method respectively(P>0 05) The positive rate of the infection of Hp L was 61 6%(69/112)in cancer group The positive rates of PCNA,CerbB 2,P 53 were significantly higher in cancer group than that in normal group(P<0 05) In cancer group,the expression of PCNA,CerbB 2,P 53 were significantly higher in Hp L infection positive group than that in negative group(P<0 05) It showed that Hp L infection was correlated with EC and the expression of PCNA,CerbB 2 and P 53 in EC The increased epithelial cell proliferation may be influenced by Hp L infection and was associated with an increased risk of EC Conclusion The pathogenetic mechanism may be that Hp L infection promotes mutation of CerbB 2 gene and P 53 gene
Keywords:Esophageal neoplasms  Helicobacter pylori  L form  Proliferating cell nuclear antigen  Oncogene
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