Published online Jan 15, 2003. doi: 10.3748/wjg.v9.i1.54
Revised: March 23, 2002
Accepted: April 20, 2002
Published online: January 15, 2003
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 = 0.0253, 0.0305 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 system mutation and telomerase reactivation, and finally causes gastric cancer.