Published online Aug 14, 2015. doi: 10.3748/wjg.v21.i30.9021
Peer-review started: April 28, 2015
First decision: May 18, 2015
Revised: June 2, 2015
Accepted: July 8, 2015
Article in press: July 8, 2015
Published online: August 14, 2015
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.
Core tip: Considering the relevance of DNA repair mechanisms in the maintenance of genome integrity and the role of epigenetics in its regulation on gastric carcinogenesis, in this review, we highlight the effects of Helicobacter pylori infection on the modulation of epigenetics mechanisms regulating DNA repair pathways associated with gastric carcinogenesis.