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. 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.
Chen
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Laboratory for Cancer Research, College of Pharmacy, Rutgers, The State University of New Jersey, 164 Frelinghuysen Road, Piscataway, NJ 08854, USA.
Yang
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CS
D000230:Adenocarcinoma / Q000453:epidemiology / Q000209:etiology / Q000473:pathology* / Q000517:prevention & control; D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D004195:Disease Models, Animal; D004938:Esophageal Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000473:pathology* / Q000517:prevention & control; D005764:Gastroesophageal Reflux / Q000150:complications; D006801:Humans; D018384:Oxidative Stress
D016718:Arachidonic Acid