Mechanism
Barrett esophagus occurs due to chronic inflammation. The principal cause of the chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD). In this disease, acidic stomach, bile, small intestine and pancreatic contents cause damage to the cells of the lower esophagus. Recently, it was shown that bile acids are able to induce intestinal differentiation, in gastroesophageal junction cells, through inhibition of the Epidermal growth factor receptor (EGFR) receptor which results in inhibition of Akt, upregulation of the p50 subunit of NF-κB (NFKB1) and ultimately activation of the promotor of the homeobox gene CDX2. The latter mastergene is responsible for the expression of intestinal markers such as Guanylate cyclase 2C . This mechanism explains the selecion of HER2/neu (or ERBB2) overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction (GEJ). Researchers are unable to predict which heartburn sufferers will develop Barrett esophagus. While there is no relationship between the severity of heartburn and the development of Barrett esophagus, there is a relationship between chronic heartburn and the development of Barrett esophagus. Sometimes people with Barrett esophagus will have no heartburn symptoms at all. In rare cases, damage to the esophagus may be caused by swallowing a corrosive substance such as lye.
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