Clinical Research
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Feb 14, 2008; 14(6): 884-891
Published online Feb 14, 2008. doi: 10.3748/wjg.14.884
H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: Correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression
Valeska Portela Lima, Marcos Antonio Pereira de Lima, Angela Rosa André, Márcia Valéria Pitombeira Ferreira, Marcos Aurélio Pessoa Barros, Sílvia Helena Barem Rabenhorst
Valeska Portela Lima, Marcos Antonio Pereira de Lima, Angela Rosa André, Márcia Valéria Pitombeira Ferreira, Sílvia Helena Barem Rabenhorst, Departament of Pathology and Forensic , Federal University of Ceará State, Brazil
Marcos Aurélio Pessoa Barros, Saint House of Mercy in Fortaleza, Brazil
Author contributions: Lima VP, de Lima MAP, André AR, Rabenhorst SHB designed research and performed research; Ferreira MVP, and Barros MAP contributed new reagents/analytic tools; de Lima MAP, analyzed data; and Lima VP, de Lima MAP, Rabenhorst SHB wrote the paper.
Correspondence to: Valeska Portela Lima, Department of Pathology and Forensic Medicine, Alexander Baraúna Street, 949 Porangabussu campus, Fortaleza, Ceará State, 60183-630 Brazil.
Telephone: +55-85-88050432
Fax: +55-85-32673840
Received: September 5, 2007
Revised: December 19, 2007
Published online: February 14, 2008

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.

Keywords: Gastric carcinoma, Helicobacter pylori, Epstein-Barr virus, p53, Bax, Bcl-2, c-Myc