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

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.

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