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World J Gastroenterol. Apr 14, 2014; 20(14): 3916-3926
Published online Apr 14, 2014. doi: 10.3748/wjg.v20.i14.3916
DNA methylation in gastric cancer, related to Helicobacter pylori and Epstein-Barr virus
Keisuke Matsusaka, Sayaka Funata, Masashi Fukayama, Atsushi Kaneda
Keisuke Matsusaka, Sayaka Funata, Atsushi Kaneda, Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan
Sayaka Funata, Masashi Fukayama, Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8654, Japan
Atsushi Kaneda, CREST, Japan Science and Technology Agency, Saitama 332-0012, Japan
Author contributions: Matsusaka K, Funata S and Kaneda A wrote the manuscript; Fukayama M and Kaneda A supervised the study.
Correspondence to: Atsushi Kaneda, MD, PhD, Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba-City 260-8670, Japan. kaneda@chiba-u.jp
Telephone: +81-43-2262039 Fax: +81-43-2262039
Received: October 28, 2013
Revised: January 8, 2014
Accepted: February 16, 2014
Published online: April 14, 2014
Processing time: 167 Days and 21.6 Hours
Core Tip

Core tip: Recent technological advances in genome-wide analysis tools have revealed various molecular aberrations in cancer. Although gastric cancer involves multiple genetic and epigenetic alterations, aberrant DNA methylation in gene promoter regions is thought to play a critical role in gastric carcinogenesis. From the etiological viewpoint, two pathogens, Helicobacter pylori (H. pylori) and Epstein-Barr virus (EBV), are known to participate in gastric carcinogenesis. Chronic inflammation in the gastric mucosa due to H. pylori and EBV infection of gastric epithelial cells has been reported to cause aberrant promoter methylation, which may contribute to the tumorigenic mechanisms of these pathogens.