Gastric adenocarcinoma and Helicobacter pylori: Correlation with p53 mutation and p27 immunoexpression |
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Authors: | Angela Rosa André Márcia Valéria Pitombeira Ferreira Rosa Maria Salani Mota Adriana Camargo Ferrasi Maria Inês de Moura Campos Pardini Sílvia Helena Barem Rabenhorst |
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Institution: | 1. Molecular Genetics Laboratory, Department of Pathology and Forensic Medicine, Federal University of Ceará, Rua Alexandre Baraúna, 949, Rodolfo Téofilo, CEP 60430-160, Fortaleza-CE, Brazil;2. Department of Mathematics and Applied Statistics, Federal University of Ceará, Campus do PICI, Bloco 910, CEP 6045-760, Fortaleza-CE, Brazil;3. Molecular Biology Laboratory of Blood Transfusion Center, Botucatu Medical School, UNESP/Campus de Botucatu-Distrito de Rubião Junior s/n, CEP 18618-970, Botucatu-SP, Brazil |
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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 p27KIP1 is a hypothesized mechanism, although there is no consensus regarding the influence of H. pylori cagA(+) in the development of these genetic alterations. Goals: To verify the relationship among H. pylori infection, p53 mutations and p27Kip1 Protein (p27) expression in gastric adenocarcinomas (GA) seventy-four tissues were assayed by PCR for H. pylori and cagA presence. Mutational analysis of p53 gene was performed by single-strand conformation polymorphism (SSCP). Seventy tissues were analyzed by an immunohistochemical method for p27 expression. Results: From the samples examined, 95% (70/74) were H. pylori positive, 63% cagA(+). Altered p53 electrophoretic mobility was found in 72% of cases and significantly more frequent in the presence of cagA. Considerable reduction in p27 expression (19%) was found with a tendency for association between cagA(+) and p27(?), although the results were not statistically significant. Concomitant alterations of both suppressor genes were detected in 60% of cases. In the cases cagA(+), 66.7% of them had these concomitant alterations. Conclusions: The data suggest that H. pylori cagA(+) contributes to p53 alteration and indicate that concomitant gene inactivation, with reduced p27 expression, may be a mechanism in which H. pylori can promote the development and progression of gastric cancer. |
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