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Combinatorial epigenetic deregulation by Helicobacter pylori and Epstein–Barr virus infections in gastric tumourigenesis
Author(s) -
Wu William KK,
Yu Jun,
Chan Matthew TV,
To Ka F,
Cheng Alfred SL
Publication year - 2016
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.4731
Subject(s) - epigenetics , biology , dna methylation , microrna , epigenomics , histone , chromatin , helicobacter pylori , cancer research , gene silencing , chromatin remodeling , cancer , genetics , cancer epigenetics , gene , gene expression , histone methyltransferase
Abstract Epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodelling and microRNAs , convert environmental signals to transcriptional outputs but are commonly hijacked by pathogenic microorganisms. Recent advances in cancer epigenomics have shed new light on the importance of epigenetic deregulation in Helicobacter pylori ‐ and Epstein–Barr virus ( EBV )‐driven gastric tumourigenesis. Moreover, it is becoming apparent that epigenetic mechanisms interact through crosstalk and feedback loops, which modify global gene expression patterns. The SWI / SNF remodelling complexes are commonly involved in gastric cancers associated with H. pylori or EBV through different mechanisms, including microRNA ‐mediated deregulation and genetic mutations. While H. pylori causes epigenetic silencing of tumour‐suppressor genes to deregulate cellular pathways, EBV ‐positive tumours exhibit a widespread and distinctive DNA hypermethylation profile. Given the early successes of epigenetic drugs in haematological malignancies, further studies are mandated to enrich and translate our understanding of combinatorial epigenetic deregulation in gastric cancers into interventional strategies in the clinic. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.