H pylori （CagA） and Epstein-Barr virus infection in gastric carcinomas：Correlation with p53 mutation and c-Myc,Bcl-2 and Bax expression

• Published in: World journal of gastroenterology : WJG 2008, Vol.14 (6), p.884-891
• Main Author: Valeska Portela Lima Marcos Antonio Pereira de Lima Angela Rosa André Márcia Valéria Pitombeira Ferreira Marcos Aurélio Pessoa Barros Sílvia Helena Barem Rabenhorst
• Format: Article
• Language: English
• Subjects: Bax; Bcl-2; p53; 幽门螺杆菌; 细菌感染
• ISSN: 1007-9327; 2219-2840

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 EBV were 94.4% and 8.45%, respectively. The majority of the cases displayed only the H pylori presence. All EBV positive 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 H pylori positive groups. CONCLUSION： The frequency of H pylori infection 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.