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World J Gastroenterol. 2014 Apr 14;20(14):3916-26. doi: 10.3748/wjg.v20.i14.3916.

DNA methylation in gastric cancer, related to Helicobacter pylori and Epstein-Barr virus.

Author information

1
Keisuke Matsusaka, Sayaka Funata, Atsushi Kaneda, Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.

Abstract

Gastric cancer is a leading cause of cancer death worldwide, and significant effort has been focused on clarifying the pathology of gastric cancer. In particular, the development of genome-wide analysis tools has enabled the detection of genetic and epigenetic alterations in gastric cancer; for example, aberrant DNA methylation in gene promoter regions is thought to play a crucial role in gastric carcinogenesis. The etiological viewpoint is also essential for the study of gastric cancers, and two distinct pathogens, Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV), are known to participate in gastric carcinogenesis. Chronic inflammation of the gastric epithelium due to H. pylori infection induces aberrant polyclonal methylation that may lead to an increased risk of gastric cancer. In addition, EBV infection is known to cause extensive methylation, and EBV-positive gastric cancers display a high methylation epigenotype, in which aberrant methylation extends to not only Polycomb repressive complex (PRC)-target genes in embryonic stem cells but also non-PRC-target genes. Here, we review aberrant DNA methylation in gastric cancer and the association between methylation and infection with H. pylori and EBV.

KEYWORDS:

DNA methylation; Epigenetics; Epstein-Barr virus; Gastric cancer; Helicobacter pylori

PMID:
24744581
PMCID:
PMC3983447
DOI:
10.3748/wjg.v20.i14.3916
[Indexed for MEDLINE]
Free PMC Article

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