Review
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Nov 21, 2006; 12(43): 6933-6940
Published online Nov 21, 2006. doi: 10.3748/wjg.v12.i43.6933
Methylation in esophageal carcinogenesis
Da-Long Wu, Feng-Ying Sui, Xiao-Ming Jiang, Xiao-Hong Jiang
Da-Long Wu, Feng-Ying Sui, Xiao-Ming Jiang, Xiao-Hong Jiang, Department of Pharmacology, School of Medicine, College of Jiaxing, Jiaxing 314001, Zhejiang Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Da-Long Wu, Department of Pharmacology, School of Medicine, College of Jiaxing, Jiaxing 314001, Zhejiang Province, China. wudalong66@sina.com
Telephone: +86-573-3643836 Fax: +86-573-3643497
Received: July 4, 2006
Revised: July 12, 2006
Accepted: July 18, 2006
Published online: November 21, 2006
Abstract

Genetic abnormalities of proto-oncogenes and tumor suppressor genes have been demonstrated to be changes that are frequently involved in esophageal cancer pathogenesis. However, hypermethylation of CpG islands, an epigenetic event, is coming more and more into focus in carcinogenesis of the esophagus. Recent studies have proved that promoter hypermethylation of tumor suppressor genes is frequently observed in esophageal carcinomas and seems to play an important role in the pathogenesis of this tumor type. In this review, we will discuss current research on genes that are hypermethylated in human esophageal cancer and precancerous lesions of the esophagus. We will also discuss the potential use of hypermethylated genes as targets for detection, prognosis and treatment of esophageal cancer.

Keywords: Methylation; Esophageal cancer; Tumor suppressor gene; Carcinogenesis