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Helicobacter pylori infection generated gastric cancer through p53-Rb tumor-suppressor system mutation and telomerase reactivation 被引量:39

Helicobacterpyloriinfection generated gastric cancer through p53-Rb tumor-suppressor system mutation and telomerase reactivation
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摘要 AIM: To investigate the relationship between Helicobacterpylori (H. pylori) infection and the expressions of the p53,Rb, c-myc, bcl-2 and hTERT mRNA in a series of diseasesfrom chronic gastritis (CG), intestinal metaplasia type Ⅰ or Ⅱ(IMⅠ-Ⅱ), intestinal metaplasia type Ⅲ (IMⅢ), mild or modestdysplasia (DysⅠ-Ⅱ), severe dysplasia (DysⅢ) to gastric cancer(GC) and to elucidate the mechanism of gastriccarcinogenesis relating to H.pyloriinfection.METHODS: 272 cases between 1998 and 2001 wereavailable for the study including 42 cases of CG, 46 cases ofIMⅠ-Ⅱ, 25 cases of IMⅢ, 48 cases of DysⅠ-Ⅱ, 27 cases ofDysⅢ, 84 cases of GC.-H. pyloriinfection and the expressionsof p53, Rb, c-myc, bcl-2 were detected by means ofstreptavidin-peroxidase (SP) immunohistochemical method.HTERT mRNA was detected byin situ hybridization(ISH).RESULTS: The expressions of p53, Rb, c-myc, hTERT mRNAand bcl-2 were higher in the GC than in CG, IN, Dys. Theexpression of c-myc was higher in IMⅢ with-H.pyloriinfection(10/16) than that without infection (1/9) and the positive ratein DysⅠ-Ⅱ and DysⅢ with-H.pyloriinfection was 18/30 and 13/17, respectively, higher than that without infection (4/18 and3/10, respectively). In our experiment mutated p53 had noassociation with H.pyloriinfection, theexpression of Rb wasassociated with-H. pyloriinfection in GC, but the p53-Rb tumor-suppressor system abnormal in DysⅠ-Ⅱ cases, DysⅢⅡ and GCcases with H. pyloriinfection was 21/30, 15/17 and 48/48respecively, higher than non-infection groups (4/18, 3/10, 28/36). Furthermore the level of hTERT mRNA in GC with H. pyloriinfection (47/48) was higher than that without infection (30/36), however the relationship between bcl-2 and H. pyloriwasonly in IMⅢ. C-myc had a close association with hTERT mRNAin DysⅢ and GC (P=0.0 253,0.0 305 respectively).CONCLUSION: In the gastric carcinogenesis, H. pylorimightcause the severe imbalance of proliferation and apoptosisin the precancerous lesions (IMⅢ and GysⅢ) first, leadingt AIM:To investigate the relationship between Helicobacter pylori(H.pylori)infection and the expressions of the p53, Rb,c-myc,bcl-2 and hTERT mRNA in a series of diseases from chronic gastritis(CG),intestinal metaplasia type Ⅰ or Ⅱ (IMⅠ-Ⅱ),intestinal metaplasia type Ⅲ(IMⅢ),mild or modest dysplasia(DysⅠ-Ⅱ),severe dysplasia(DysⅢ)to gastric cancer (GC)and to elucidate the mechanism of gastric carcinogenesis relating to H.pylori infection. METHODS:272 cases between 1998 and 2001 were available for the study including 42 cases of CG,46 cases of IMⅠ-Ⅱ,25 cases of IMⅢ,48 cases of DysⅠ-Ⅱ,27 cases of DysⅢ,84 cases of GC.H.pylori infection and the expressions of p53,Rb,c-myc,bcl-2 were detected by means of streptavidin-peroxidase(SP)immunohistochemical method. HTERT mRNA was detected by in situ hybridization(ISH). RESULTS:The expressions of p53,Rb,c-myc,hTERT mRNA and bcl-2 were higher in the GC than in CG,IM,Dys.The expression of c-myc was higher in IMⅢ with H.pylori infection (10/16)than that without infection(1/9)and the positive rate in DysⅠ-Ⅱ and DysⅢ with H.pylori infection was 18/30 and 13/ 17,respectively,higher than that without infection(4/18 and 3/10,respectively).In our experiment mutated p53 had no association with H.pylori infection,the expression of Rb was associated with H.pylori infection in GC,but the p53-Rb tumor- suppressor system abnormal in DysⅠ-Ⅱ cases,DysⅢ and GC cases with H.pylori infection was 21/30,15/17 and 48/48 respecively,higher than non-infection groups(4/18,3/10,28/ 36).Furthermore the level of hTERT mRNA in GC with H.pylori infection(47/48)was higher than that without infection(30/ 36),however the relationship between bcl-2 and H.pylori was only in IMⅢ.C-myc had a close association with hTERT mRNA in DysⅢ and GC(P=0.0 253,0.0 305 respectively). CONCLUSION:In the gastric carcinogenesis,H.pylori might cause the severe imbalance of proliferation and apoptosis in the precancerous lesions(IMⅢ and GysⅢ)first,leading to p53-Rb tumor-suppressor sy
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2003年第1期54-58,共5页 世界胃肠病学杂志(英文版)
基金 the National Science Fund of Hubei Province,No. 98J087 the Department of Health of Hubei Province,No.WJ01572
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