Gastric carcinogenesis has been studied in various aspects. Helicobacter pylori (Hp) infection and mutation of the p53 tumor suppressor gene have recently been argued to be important factors of gastric carcinogenesis. There have been many studies to determine the precise mechanism of how Hp is related to gastric cancer, but it is so far still unknown. We studied the relationship of Hp infection and p53 overexpression and tried to discover some significance in clinicopathologic factors such as age, sex, stage, site, differentiation and gross morphology. Ninety-six patients who were diagnosed with gastric cancer at Severance Hospital, Yonsei University Medical College from November 1995 to March 1996, and 96 control patients of non-ulcer dyspepsia (NUD) were studied by endoscopic biopsy of normal gastric tissue and cancer tissue. They also underwent the CLO® (Delta West, Melbourne, Western Australia) test for Hp positivity and p53 immunohistochemical stain for p53 positivity. These data were analyzed for comparison with the clinicopathologic characteristics of gastric cancers. In conclusion, the differentiated group cancer had a significantly high Hp positivity and p53 positivity. There is a possibility that Hp infection and p53 tumor suppressor gene mutation might be significantly related in the gastric carcinogenic process of well- and moderately-differentiated adenocarcinomas, but further study is necessary to determine more direct clues on the carcinogenic roles of these factors.
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