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Barrett esophagus (BE) is a human metaplastic condition that is the only known precursor to esophageal adenocarcinoma. BE is characterized by a posterior intestinal-like phenotype in an anterior organ and therefore it is reminiscent of homeotic transformations, which can occur in transgenic animal models during embryonic development as a consequence of mutations inHOX genes. In humans, acquired deregulation ofHOX genes during adulthood has been linked to carcinogenesis; however, little is known about their role in the pathogenesis of premalignant conditions. We hypothesized thatHOX genes may be implicated in the development of BE. We demonstrated that three midclusterHOXB genes (HOXB5 ,HOXB6 , andHOXB7 ) are overexpressed in BE, compared with the anatomically adjacent normal esophagus and gastric cardia. The midclusterHOXB gene signature in BE is identical to that seen in normal colonic epithelium. Ectopic expression of these three genes in normal squamous esophageal cells in vitro induces markers of intestinal differentiation, such asKRT20 ,MUC2 , andVILLIN . In BE-associated adenocarcinoma, the activation midclusterHOXB gene is associated with loss of H3K27me3 and gain of AcH3, compared with normal esophagus. These changes in histone posttranslational modifications correlate with specific chromatin decompaction at theHOXB locus. We suggest that epigenetically regulated alterations ofHOX gene expression can trigger changes in the transcriptional program of adult esophageal cells, with implications for the early stages of carcinogenesis.

Evidence for a functional role of epigenetically regulated midclusterHOXBgenes in the development of Barrett esophagus