From genetics to signaling pathways: molecular pathogenesis of esophageal adenocarcinoma

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...

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Bibliographic Details
Published in:Biochimica et biophysica acta. Reviews on cancer 2019-08, Vol.1872 (1), p.37-48
Main Authors: Caspa Gokulan, Ravindran, Garcia-Buitrago, Monica T., Zaika, Alexander I.
Format: Article
Language:English
Subjects:
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Barrett Esophagus - genetics
Barrett Esophagus - pathology
Barrett’s esophagus
DNA Damage - genetics
Esophageal adenocarcinoma
Esophageal cancer
Esophageal Neoplasms - genetics
Esophageal Neoplasms - pathology
Gastroesophageal Reflux - genetics
Gastroesophageal Reflux - pathology
GERD
Humans
p53
Risk Factors
Signal Transduction - genetics
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Summary: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.
ISSN:0304-419X
1879-2561
DOI:10.1016/j.bbcan.2019.05.003