From genetics to signaling pathways: molecular pathogenesis of esophageal adenocarcinoma

Research output: Contribution to journalReview article

2 Scopus citations

Abstract

Esophageal adenocarcinoma (EAC) has one of the fastest rising incidence rates in the U.S. and many other Western countries. One of the unique risk factors for EAC is gastroesophageal reflux disease (GERD), a chronic digestive condition in which acidic contents from the stomach, frequently mixed with duodenal bile, enter the esophagus resulting in esophageal tissue injury. At the cellular level, progression to EAC is underlined by continuous DNA damage caused by reflux and chronic inflammatory factors that increase the mutation rate and promote genomic instability. Despite recent successes in cancer diagnostics and treatment, EAC remains a poorly treatable disease. Recent research has shed new light on molecular alterations underlying progression to EAC and revealed novel treatment options. This review focuses on the genetic and molecular studies of EAC. The molecular changes that occur during the transformation of normal Barrett's esophagus to esophageal adenocarcinoma are also discussed.

Original languageEnglish (US)
Pages (from-to)37-48
Number of pages12
JournalBiochimica et Biophysica Acta - Reviews on Cancer
Volume1872
Issue number1
DOIs
StatePublished - Aug 1 2019

Keywords

  • Barrett's esophagus
  • Esophageal adenocarcinoma
  • Esophageal cancer
  • GERD
  • p53

ASJC Scopus subject areas

  • Oncology
  • Genetics
  • Cancer Research

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