Gastric adenocarcinoma and Helicobacter pylori: correlation with p53 mutation and p27 immunoexpression.

Introduction: Helicobacter pylori infection is an established risk factor for gastric cancer development, but the exact underlying mechanism still remains obscure. The inactivation of tumor suppressor genes such as p53 and p27(KIP1) is a hypothesized mechanism, although there is no consensus regarding the influence of H. pylori cagA(+) in the development of these genetic alterations.

p27KIP1 expression in gastric cancer: differential pathways in the histological subtypes associated with Helicobacter pylori infection.

Objective: Decreases in p27(KIP1) and C-MYC expression have been associated with Helicobacter pylori infection. Furthermore, C-MYC seems to be a transcriptional repressor of p27(KIP1). Therefore, in a series of gastric adenocarcinomas we studied the association of p27(KIP1) expression with H.

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

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.