Cellular origins and molecular mechanisms of Barrett's esophagus and esophageal adenocarcinoma

This paper presents commentaries on animal models used for Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) research; acid‐ and bile‐induced chromosomal instability and clonal selection during the progression of BE to EAC; how the components of gastric refluxate, especially acid and bile salts, promote carcinogenesis in metaplastic BE; genome‐wide changes in DNA methylation and transcription involved in BE carcinogenesis; the potential role of miRNA in the development of BE and EAC; the effect of inflammatory cytokines linked to obesity on the activation of cell‐death pathways and cell survival in BE and esophageal cancer; and the role of autophagy in esophageal cancer development.