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Helicobacter pylori and EBV in gastric carcinomas: Methylation status and microsatellite instability

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Author(s): Adriana Camargo Ferrasi, Nídia Alice Pinheiro, Silvia Helena Barem Rabenhorst, Otávia Luisa Caballero, Maria Aparecida Marchesan Rodrigues, Fabrício Carvalho, Celso Vieira Souza Leite, Marcia Valéria Pitombeira Ferreira, Marcos Aurélio Pessoa Barros, Maria Inês Moura Campos Pardini

Journal: World Journal of Gastroenterology
ISSN 1007-9327

Volume: 16;
Issue: 3;
Start page: 312;
Date: 2010;
Original page

Keywords: Gastric cancer | Methylation | Microsatellite instability | Helicobacter pylori | Epstein Barr virus

ABSTRACT
AIM: To verify the methylation status of CDH1, DAPK, COX2, hMLH1 and CDKN2A genes and to evaluate their association with Helicobacter pylori (H. pylori)-cagA+ and Epstein Barr virus (EBV) infections in gastric adenocarcinomas.METHODS: Methylation-specific PCR (MSP) assay was performed in 89 primary gastric carcinomas (intestinal and diffuse types). Microsatellite instability (MSI) analysis was performed using the BAT26 primer set and PCR products were analyzed with the ABI PRISM 3100 Genetic Analyzer using Genescan 3.7 software (Applied Biosystems). Detection of H. pylori and genotyping were performed by PCR, using specific primers for ureaseC and cagA genes. The presence of EBV was assessed by in situ hybridization. Statistical analyses were performed using the χ2 or Fisher’s exact test.RESULTS: The most frequent hypermethylated gene was COX-2 (63.5%) followed by DAPK (55.7%), CDH1 (51%), CDKN2A (36%) and hMLH1 (30.3%). Intestinal and diffuse adenocarcinomas showed different methylation profiles and there was an association between methylation of E-CDH1 and H. pylori-cagA+ in the intestinal adenocarcinoma type. MSI was correlated with hMLH1 methylation. There was an inverse correlation between DAPK hypermethylation and MSI.CONCLUSION: We found a strong association between CDH1 methylation and H. pylori-cagA+ in intestinal-type gastric cancer, association of MSI and better prognosis and an heterogeneous COX-2 overexpression.

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