Gastric adenocarcinoma and Helicobacter pylori: Correlation with p53 mutation and p27 immunoexpression

摘要: Abstract 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 a hypothesized mechanism, although there no consensus regarding influence H. cagA (+) in development these genetic alterations. Goals: To verify relationship among infection, mutations Kip1 Protein (p27) expression adenocarcinomas (GA) seventy-four tissues were assayed by PCR presence. Mutational analysis gene was performed single-strand conformation polymorphism (SSCP). Seventy analyzed immunohistochemical method expression. Results: From samples examined, 95% (70/74) positive, 63% (+). Altered electrophoretic mobility found 72% cases significantly more frequent presence . Considerable reduction (19%) with tendency association between p27(−), results not statistically significant. Concomitant alterations both detected 60% cases. In (+), 66.7% them had concomitant Conclusions: data suggest that contributes to alteration indicate inactivation, reduced expression, may be which can promote progression cancer.