Are you Marcos Antonio Pereira de Lima?

Claim your profile

Publications (2)4.64 Total impact

  • Article: The relationship between Helicobacter pylori genes cagE and virB11 and gastric cancer.
    [show abstract] [hide abstract]
    ABSTRACT: The association between Helicobacter pylori gene diversity and gastric cancer has been poorly reported, although it is one of the important ways to explain the gastric pathogenesis. The aim of this study was to investigate the frequency of cagE and virB11 genes in H. pylori isolated from patients with gastric cancer and to analyze the histology profiles. The presence of H. pylori and subtypes (cagE and virB11) was detected by PCR from the genomic DNA of 101 patients who had been diagnosed with gastric cancer. The cases were grouped according to the presence/absence of the genes studied and were analyzed in relation to histopathological parameters. H. pylori infection was detected in 94 out of 101 (93.1%) gastric carcinomas. The cases were categorized into the following groups: cagE+/virB11+, cagE+/virB11-, cagE-/virB11+, and cagE-/virB11-. Frequencies were: 50% (47/94) cagE+/virB11+, 3.2% (3/94) cagE+/virB11-, 10.6% (10/94) cagE-/virB11+, and 36.2% (34/94) cagE-/virB11-. Tumors in the gastric antrum were predominant. An exception was the cagE-/virB11- group, in which tumors had a tendency to be located in the gastric cardia; the majority of the cardia tumors (56% (14/25)) were in this group. Intestinal histology type was the most frequent, but the cagE+/virB11- group only had diffuse tumors. H. pyloricagE+/virB11+ occurred most frequently (except at stage III), and was present at all gastric cancer stages. This study is the first to include a relevant number of gastric cancer cases with H. pylori infection, reporting the frequency and relationship of cagE and virB11 genes and the genesis of this tumor. The presence of these cag pathogenicity island genes shows that they are important factors for the pathogenesis and malignancy of gastric cancer related to H. pylori.
    International journal of infectious diseases: IJID: official publication of the International Society for Infectious Diseases 07/2010; 14(7):e613-7. · 2.17 Impact Factor
  • Article: H pylori (CagA) and Epstein-Barr virus infection in gastric carcinomas: correlation with p53 mutation and c-Myc, Bcl-2 and Bax expression.
    [show abstract] [hide abstract]
    ABSTRACT: 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. 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. 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. 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.
    World Journal of Gastroenterology 03/2008; 14(6):884-91. · 2.47 Impact Factor