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The authors declare that they have no competing interests. Authors’ contributions XZ did the MTT essay and immunohistochemistry, XS did the Cell-culturing, submitted paper and revised the paper, FG did the medical statistics, JL cultured the cell and did PCR, ZS designed this experiment and wrote this paper. All authors read and approved this final draft.”
“Introduction Esophageal adenocarcinoma (EAC) is an entity of increasing clinical importance, due to an unexplained incidence rise among white eltoprazine males in the Western world [1], and a dismal prognosis [2, 3]. Chances for cure are still limited to early, surgically resectable tumor stages, prior to systemic dissemination of the disease. EACs develop almost exclusively in the distal third of the esophagus, under the chronically damaging effect of gastroesophageal reflux [2, 3]. Barrett’s esophagus (BE) – defined as columnar-lined epithelium in the distal esophagus, characterized by specialized intestinal mucosa (with goblet cells) – is regarded as a precancerous lesion, giving rise to these tumors. Malignant progression within BE is regarded to follow a sequence of well-characterized histopathologic changes, from intestinal metaplasia, over low-grade and high-grade dysplasia/intraepithelial neoplasia towards invasive adenocarcinomas [2, 3].