| Background and Objective: Gastric carcinoma is the most common malignant tumor. Helicobacter pylori (Hp) is to be thought as a trigger of gastric carcinoma. But the mechanism of Hp inducing gastric carcinoma is not clear. Mismatch repair (MMR) genes are conservative housekeeping genes, whose function is to repair the mismatch of nucleotide in DNA replication. Any abnormal expressions of MMR genes and their products may lead to the absence of MMR functions and furthermore cellular malignant transformation. The products of suppressor genes can inhibit immoderate growth of cells and their absence also makes a cause of cellular malignant transformation. It is not known whether Hp induce the occurrence of gastric carcinoma by inhibiting the functions of MMR genes and suppressor genes? This study is designed to answer the question by analyzing the relationship of Hp infection to expressions of MMR genes (hMLH1, hMSH2) and suppressor genes (p53, PTEN) in gastric epithelia of chronic gastritis (gastritis group), carcinoma cells(carcinoma group) and the epithelia surrounding carcinomas (surrounding group), and then to explain the possible carcinogenesis induced by Hp infection.Materials and methods: Gastric biopsy specimens of 34 gastritis and 62 gastric carcinoma with their surrounding epithelia were got with endoscopy from 2002 to 2003 in the first affiliated hospital of Dalian medical university. Guick-ureolytase method was used to detect Hp infection and the immunohistochemical method was used to examine the product expressions of MMR genes (hMLH1, hMSH2) and suppressor genes (p53, PTEN) in epithelial cells from gastritis, carcinoma and surrounding groups. Chi-square is used for statistic analysis.Results: Hp infection rates were 64.7% (22/34) in gastritis group and 48.3% (30/62) in carcinoma group, respectively.The positive rate of hMLH1expression in gastritis group being 32.4% (11/34) was significantly lower than that in surrounding group being 88.7% (55/62) (P<0.05) and that in carcinoma group being 83.9% (52/62) (P<0.05), while there was not different between surrounding group and carcinoma group (P>0.05). The positive rate of hMSH2 expression was 52.9% (18/34) in gastritis group and 54.8% (34/62) in surrounding group, but both of two groups were significantly lower than that in carcinoma group being 80.6% (50/62) (P<0.05). The positive rate of P53 expression was 23.5% (8/34) in gastritis group and was 11.3% (7/62) in surrounding group, but both of two groups were significantly lower than that in carcinoma group being 88.7% (55/62) (P<0.05). The positive rate of PTEN expression was 91.2% (31/34) in gastritis group and was 75.8% (47/62) in surrounding group, but was 64.5% (40/62) in carcinoma group which was significantly lower than that in gastritis group (P <0.05). The positive rates of hMLH1expression in gastritis group, surrounding group and carcinoma group with Hp infection were 36.4% (8/22), 86.7% (26/30) and 80.0% (24/30), respectively. Those without Hp infection were 25.0% (3/12), 90.6% (29/32) and 87.5% (28/32), respectively. There was not significantly different in hMLH1 expression between the groups with and without Hp infection (P>0.05). The positive rates of hMSH2 expression in gastritis group with Hp infection and without were 50.0% (11/22) and 58.3% (7/12), respectively (P>0.05). The positive rates of hMSH2 expression in surrounding group with Hp infection and without were 53.3% (16/30) and 56.3% (18/32), respectively (P>0.05). The positive rate of hMSH2 expression in carcinoma group with Hp infection being 70.0% (21/30) was significantly lower than that without Hp infection being 90.6% (29/32) (P<0.05). The positive rate of P53 expression in gastritis group with Hp infection being 18.2% (4/22) was lower than that without Hp infection being 33.3% (4/12) (P>0.05). The positive rate of P53 expression in surrounding group with Hp infection being 6.7% (2/30) was lower than that without Hp infection being 15.6% (5/32) (P>0.05). The positive rate of P53 expression in carcinoma g... |
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