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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.pylori infection.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.pylori infection and the expressionsof p53,Rb,c-myc,bcl-2 were detected by means ofstreptavidin-peroxidase(SP)immunohistochemical method.HTERT mRNA was detected by in situ hybridization(ISH).RESULTS:The expressions of p53,Rb,c-myc,hTERT mRNAand bcl-2 were higher in the GC than in CG,IM,Dys.Theexpression of c-myc was higher in IMⅢ with H.pylori infection(10/16)than that without infection(1/9)and the positive ratein DysⅠ-Ⅱ and DysⅢ with H.pylori infection 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.pylori infection,the expression of Rb wasassociated with H.pylori infection in GC,but the p53-Rb tumor-suppressor system abnormal in DysⅠ-Ⅱ cases,DysⅢ and GCcases with H.pylori infection 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.pylori wasonly 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.pylori mightcause the severe imbalance of proliferation and apoptosisin the precancerous lesions(IMⅢ and GysⅢ)first,leadingto p53-Rb tumor-suppressor system mutation and telomerasereactivation,and finally causes gastric cancer.
A 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 modestdysplasia (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 IM I-II, 25 cases of IM III, 48 cases of Dys I-II, 27 cases of Dys III, 84 cases of GC. H. pylori infection and the expressionsof Results: p53, Rb, c-myc and bcl-2 were detected by means of streptavidin-peroxidase (SP) immunohistochemical method. HRT 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. Theexpression of c-myc was higher in IMIII with H.pylori infection (10/1 6) than that without infection (1/9) and the positive rate of Dys I-II and Dys III 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 wasassociated with H. pylori infection in GC, but the p53-Rb tumor-suppressor system abnormal in Dys I-II cases, Dys III and GCcases with H. (4 / 18,3 / 10,28 / 36) .Furthermore the level of hTERT mRNA in GC with H.pylori infection (47/48 / 48respecively, higher than non-infection groups 48) was higher than that without infection (30/36), however the relationship between bcl-2 and H. pylori was inly in IM III. C-myc had a close association with hTERT mRNAin Dys III and GC (P = 0.0253,0.0305 respectively. CONCLUSION: In the gastric carcinogenesis, H. pylori mightcause the severe imbalance of proliferation and apoptosis in the precancerous lesions (IM III and Gys III) first, leadingto p53-Rb tumor- suppressor system mutation and telomerasereactivation, and finally causes gastric cancer.