Methylation in esophageal carcinogenesis

World J Gastroenterol. 2006 Nov 21;12(43):6933-40. doi: 10.3748/wjg.v12.i43.6933.

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.

Publication types

  • Review

MeSH terms

  • CpG Islands / genetics
  • DNA Methylation*
  • DNA, Neoplasm / blood
  • Esophageal Neoplasms / etiology*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / metabolism*
  • Humans
  • Prognosis
  • Promoter Regions, Genetic / genetics

Substances

  • DNA, Neoplasm