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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: Exp Biol Med (Maywood). 2014 Apr 29;239(9):1108–1123. doi: 10.1177/1535370214529388

Figure 3.

Figure 3

Model for progression from GERD to BE to EAC. Illustration summarizing the transition from normal esophageal epithelium to metaplastic Barrett’s esophagus (BE) to esophageal adenocarcinoma (EAC). Following reflux injury, epithelial cells experience several genetic events that, when combined with microenvironmental signals from stromal fibroblasts and infiltrating immune cells, trigger the development of intestinal columnar cells in place of stratified epithelium. BE is a precursor lesion that will continue to accumulate molecular alterations, ultimately leading to the development of dysplasia and invasive EAC.