Esophageal adenocarcinoma: a review and perspectives on the mechanism of carcinogenesis and chemoprevention

The incidence rate of esophageal adenocarcinoma (EAC) has increased sharply in the past 30 years. Many risk factors have been identified and gastroesophageal reflux disease (GERD) is the most important one. Columnar-lined esophagus, resulting from GERD, is recognized as a key precursor lesion of EAC...

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Bibliographic Details
Published in:Carcinogenesis (New York) 2001-08, Vol.22 (8), p.1119-1129
Main Authors: Chen, Xiaoxin, Yang, Chung S.
Format: Article
Language:English
Subjects:
2-DE
Adenocarcinoma - epidemiology
Adenocarcinoma - etiology
Adenocarcinoma - pathology
Adenocarcinoma - prevention & control
Animal tumors. Experimental tumors
Animals
Arachidonic Acid - metabolism
Biological and medical sciences
CLE
columnar-lined esophagus
Cox
cyclooxygenase
Disease Models, Animal
EAC
EDA
EGDA
esophageal adenocarcinoma
Esophageal Neoplasms - epidemiology
Esophageal Neoplasms - etiology
Esophageal Neoplasms - pathology
Esophageal Neoplasms - prevention & control
esophagoduodenal anastomosis
esophagogastroduodenal anastomosis
Esophagus
Experimental digestive system and abdominal tumors
Gastroenterology. Liver. Pancreas. Abdomen
Gastroesophageal Reflux - complications
gastroesophageal reflux disease
GERD
Humans
inducible nitric oxide synthase
iNOS
leukotriene
leukotriene A4 hydrolase
lipoxygenase
Lox
LTA4H
Medical sciences
non-steroidal anti-inflammatory drugs
NSAIDs
Oxidative Stress
phospholipase A2
PLA2
prostaglandin
reactive oxygen species
ROS
Tumors
two-dimensional gel electrophoresis
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Description
Summary:The incidence rate of esophageal adenocarcinoma (EAC) has increased sharply in the past 30 years. Many risk factors have been identified and gastroesophageal reflux disease (GERD) is the most important one. Columnar-lined esophagus, resulting from GERD, is recognized as a key precursor lesion of EAC. In this article, we review the studies on EAC in humans and animal models. We propose that the pathogenesis of EAC is mainly driven by inflammation and oxidative stress, which are augmented by iron overload. The overproduction of prostaglandin E2 and leukotriene B4 and overexpression of their receptors are believed to be major factors in exacerbating inflammation and oxidative stress. Based on this mechanistic understanding, antioxidants, inhibitors of arachidonic acid metabolism enzymes and receptor antagonists of certain eicosanoids are proposed as potential chemopreventive agents for EAC in future studies.
ISSN:0143-3334
1460-2180
1460-2180
DOI:10.1093/carcin/22.8.1119