Journal Article

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

Xiaoxin Chen and Chung S. Yang

in Carcinogenesis

Volume 22, issue 8, pages 1119-1129
Published in print August 2001 | ISSN: 0143-3334
Published online August 2001 | e-ISSN: 1460-2180 | DOI:
Esophageal adenocarcinoma: a review and perspectives on the mechanism of carcinogenesis and chemoprevention

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  • Clinical Cytogenetics and Molecular Genetics


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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.

Keywords: CLE, columnar-lined esophagus; Cox, cyclooxygenase; 2-DE, two-dimensional gel electrophoresis; EAC, esophageal adenocarcinoma; EDA, esophagoduodenal anastomosis; EGDA, esophagogastroduodenal anastomosis; GERD, gastroesophageal reflux disease; iNOS, inducible nitric oxide synthase; Lox, lipoxygenase; LT, leukotriene; LTA4H, leukotriene A4 hydrolase; NSAIDs, non-steroidal anti-inflammatory drugs; PG, prostaglandin; PLA2, phospholipase A2; ROS, reactive oxygen species.

Journal Article.  10790 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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