Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Epigenetic Regulation Of Dna Repair Machinery In Helicobacter Pylori-induced Gastric Carcinogenesis
Author: Santos
Juliana Carvalho; Ribeiro
Marcelo Lima
Abstract: Although thousands of DNA damaging events occur in each cell every day, efficient DNA repair pathways have evolved to counteract them. The DNA repair machinery plays a key role in maintaining genomic stability by avoiding the maintenance of mutations. The DNA repair enzymes continuously monitor the chromosomes to correct any damage that is caused by exogenous and endogenous mutagens. If DNA damage in proliferating cells is not repaired because of an inadequate expression of DNA repair genes, it might increase the risk of cancer. In addition to mutations, which can be either inherited or somatically acquired, epigenetic silencing of DNA repair genes has been associated with carcinogenesis. Gastric cancer represents the second highest cause of cancer mortality worldwide. The disease develops from the accumulation of several genetic and epigenetic changes during the lifetime. Among the risk factors, Helicobacter pylori (H. pylori) infection is considered the main driving factor to gastric cancer development. Thus, in this review, we summarize the current knowledge of the role of H. pylori infection on the epigenetic regulation of DNA repair machinery in gastric carcinogenesis.
Subject: Base Excision-repair
Histone H2ax Phosphorylation
Squamous-cell Carcinoma
Double-strand Breaks
Microsatellite Instability
Mismatch Repair
Promoter Hypermethylation
Citation: Epigenetic Regulation Of Dna Repair Machinery In Helicobacter Pylori-induced Gastric Carcinogenesis. Baishideng Publishing Group Inc, v. 21, p. 9021-9037 AUG-2015.
Rights: fechado
Identifier DOI: 10.3748/wjg.v21.i30.9021
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File SizeFormat 
wos_000362233700004.pdf1.48 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.