H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas:Correlation With p53 mutation

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AIM:To investigate the interrelationship between H pylori and Epstein-Barr virus(EBV)infection in the gastric carcinogenesis having in focus the p53 mutation and the c-Myc,Bcl-2 and Bax expression.METHODS:seventy-one gastric carcinoma tissues were assessed by polymerase chain reaction (PCR) for H pylori and in situ hybridization for EBV. c-Myc,Bcl-2 and Bax expression were detected by immunohistochemistry and single-stranded conformational polymorphism (SSCP) for p53 mutation.RESULTS:The positivity rates for H pylori and EBVwere 94.4% and 8.45%,respectively.The majority of the cases displayed only the H pylori presence.All EBVpositive cases were also H pylori positive.None infectious agent was observed in 5.55% of the cases.The intestinal type tumor was more frequent in the co-infected and non-infected groups.The female predominated in the non-infected group showing statistical significance (70.4% vs 29.6%, P=0.039).The Bcl-2 was only detected in the group exclusively infected by H pylori.However,c-Myc and Bax were detected in the three groups but with a low frequency in the co-infected group.Mutation of p53 was present in all groups,with the highest frequencies in the Hpylori positive groups.in gastric carcinomas was high.The presented data indicated that gastric carcinogenesis has different pathways depending of the presence of the two investigated infectious agents,suggesting a possible involvement of H pylori with apoptotic process.The low expression of c-Myc and Bax in the EBV-positive groups suggests that EBV may inhibit the expression of these proteins.Nevertheless,p53 mutation shows to be a relevant alteration,independent of both infectious agents.
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