Mechanisms of esophageal adenocarcinoma formation and approaches to chemopreventive intervention.
The incidence of esophageal adenocarcinoma (EAC), a debilitating and highly lethal malignancy, has risen dramatically over the past 40 years in the United States and other Western countries. To reverse this trend, EAC prevention and early detection efforts by clinicians, academic researchers and endoscope manufacturers have targeted Barrett's esophagus (BE), the widely accepted EAC precursor lesion. Data from surgical, endoscopic and pre-clinical investigations strongly support the malignant potential of BE. For patients with BE, the risk of developing EAC has been estimated at 11- to 125-fold greater than that of the individual at average risk. Nevertheless, screening for BE in symptomatic patients (ie, with symptoms of reflux) and surveillance in patients diagnosed with BE have not had a substantial impact on the incidence, morbidity or mortality of EAC; the overwhelming majority of EAC patients are diagnosed without a pre-operative diagnosis of BE. This article will discuss the current state of the science of esophageal adenocarcinoma prevention, including ideas about carcinogenesis and its underlying genomic and molecular level mechanisms, and suggest strategies for a systems approach to targeted preventive management.
['Richmond|Ellen|E|', 'Umar|Asad|A|']
D000230:Adenocarcinoma D000818:Animals D000894:Anti-Inflammatory Agents, Non-Steroidal D001471:Barrett Esophagus D002471:Cell Transformation, Neoplastic D018890:Chemoprevention D004938:Esophageal Neoplasms D005764:Gastroesophageal Reflux D006801:Humans D007249:Inflammation D059016:Tumor Microenvironment
Barrett’s esophagus Cell of origin Esophageal adenocarcinoma Chemoprevention Somatic evolution