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• W2000454221 startingPage "4328" @default.
• W2000454221 abstract "The incidence of esophageal adenocarcinoma (EAC) is rapidly rising in the western world and accounts for 2% of all cancer-related deaths. The precursor lesion for EAC is Barrett esophagus (BE), which is strongly associated with gastresophageal reflux disease. A major limitation to the study of EAC has been the absence of tractable and genetically modifiable preclinical models of BE. A mouse model of BE and EAC that resembles human disease could provide novel insights into the origins and molecular pathogenesis of BE. In addition, validated animal models could help stratify BE patients given the limited predictive power of current standard endoscopic measures and clinical assessment. Here, we review the findings from recently developed mouse models of BE and EAC and their impact on clinical decision making, surveillance programs and therapeutic options. The data, taken together, suggest potential origins of BE from the gastric cardia, a role of bile acid and hypergatrinemia for carcinogenesis, a growing importance for columnar-like epithelium and a critical role for Notch signaling." @default.
• W2000454221 created "2016-06-24" @default.
• W2000454221 creator A5034242696 @default.
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• W2000454221 creator A5075581309 @default.
• W2000454221 creator A5082883972 @default.
• W2000454221 date "2012-12-01" @default.
• W2000454221 modified "2023-10-03" @default.
• W2000454221 title "Barrett esophagus" @default.
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• W2000454221 doi "https://doi.org/10.4161/cc.22485" @default.
• W2000454221 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3552915" @default.
• W2000454221 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23095673" @default.
• W2000454221 hasPublicationYear "2012" @default.
• W2000454221 type Work @default.
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