Original Research
Copyright ©The Author(s) 2001. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2001; 7(6): 779-782
Published online Dec 15, 2001. doi: 10.3748/wjg.v7.i6.779
Apoptosis, proliferation and p53 gene expression of H. pylori associated gastric epithelial lesions
Zhong Zhang, Yuan Yuan, Hua Gao, Ming Dong, Lan Wang, Yue-Hua Gong
Zhong Zhang, Yuan Yuan, Hua Gao, Ming Dong, Lan Wang, Yue-Hua Gong, Department of Pathology, Shenyang Medical College, Shenyang 110031, Liaoning Province, China
Author contributions: All authors contributed equally to the work.
Supported by National Ninth Five-Year Study Program for Tacking Key Scientific Problems, No. 96-906-01-04
Correspondence to: Yuan Yuan, Cancer Institute of First Hospital, China Medical University, Shenyang 110001, Liaoning Province, China. yyuan@mail.cmu.edu.cn
Telephone: +86-24-23256666-6153
Received: June 12, 2001
Revised: July 19, 2001
Accepted: August 20, 2001
Published online: December 15, 2001

AIM: To study the relationship between Helicobacter pylori (H. pylori) and gastric carcinoma and its possible pathogenesis by H. pylori.

METHODS: DNEL technique and immunohistochemical technique were used to study the state of apoptosis, proliferation and p53 gene expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30 H. pylori-negative and 30 H. pylori-positive gastric precancerous lesions along with 20 gastric carcinomas were studied.

RESULTS: There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, there were few apoptotic cells, while there were a large number of proliferative cells, and expression of p53 protein significantly was increased. In the phase of metaplasia, the apoptotic index (AI, 4.36% ± 1.95%), proliferative index (PI, 19.11% ± 6. 79%) and positivity of p53 expression (46.7%) in H. pylori-positive group were higher than those in normal mucosa (P < 0.01). AI in H. pylori-positive group was higher than that in H. pylori-negative group (3.81% ± 1.76%), PI in H. pylori-positive group was higher than that in H. pylori-negative group (12.25% ± 5.63%, P < 0.01). In the phase of dysplasia, AI (2.31% ± 1.10%) in H. pylori-positive group was lower (3.05% ± 1.29%) than that in H. pylori-negative group, but PI (33.89% ± 11.65%) was significantly higher (22.09% ± 80.18%, P < 0.01). In phases of metaplasia, dysplasia and gastric cancer in the H. pylori-positive group, AIs had an evidently graduall decreasing trend (P < 0.01), while PIs had an evidently gradual increasing trend (P < 0.05 or P < 0.01), and there was also a trend of gradual increase in the expression of p53 gene.

CONCLUSION: In the course of the formation of gastric carcinoma, proliferation of gastric mucosa can be greatly increased by H. pylori, and H. pylori can induce apoptosis in the phase of metaplasia, but in the phase of dysplasia H. pylori can inhibit cellular apoptosis. And H. pylori infection can strengthen the expression of mutated p53 gene.

Keywords: Helicobacter pylori, gastric precancerous lesion, apoptosis, proliferation, p53 gene