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Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett-like metaplasia.

Cancer cell | Jan 17, 2012

http://www.ncbi.nlm.nih.gov/pubmed/22264787

Esophageal adenocarcinoma (EAC) arises from Barrett esophagus (BE), intestinal-like columnar metaplasia linked to reflux esophagitis. In a transgenic mouse model of BE, esophageal overexpression of interleukin-1β phenocopies human pathology with evolution of esophagitis, Barrett-like metaplasia and EAC. Histopathology and gene signatures closely resembled human BE, with upregulation of TFF2, Bmp4, Cdx2, Notch1, and IL-6. The development of BE and EAC was accelerated by exposure to bile acids and/or nitrosamines, and inhibited by IL-6 deficiency. Lgr5(+) gastric cardia stem cells present in BE were able to lineage trace the early BE lesion. Our data suggest that BE and EAC arise from gastric progenitors due to a tumor-promoting IL-1β-IL-6 signaling cascade and Dll1-dependent Notch signaling.

Pubmed ID: 22264787 RIS Download

Mesh terms: Adenocarcinoma | Animals | Barrett Esophagus | Bile Acids and Salts | Bone Morphogenetic Protein 4 | Cardia | Esophageal Neoplasms | Esophagitis | Homeodomain Proteins | Interleukin-1beta | Interleukin-6 | Metaplasia | Mice | Mice, Transgenic | Mucins | Muscle Proteins | Peptides | Receptor, Notch1 | Signal Transduction | Stem Cells | Transcription Factors | Up-Regulation

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Associated grants

  • Agency: NCI NIH HHS, Id: 1U54CA126513,
  • Agency: NCI NIH HHS, Id: 5U01 CA143056
  • Agency: NCI NIH HHS, Id: K07 CA132892
  • Agency: NCI NIH HHS, Id: K07 CA132892
  • Agency: NCI NIH HHS, Id: P01-CA098101
  • Agency: NIDDK NIH HHS, Id: P30-DK050306
  • Agency: NCI NIH HHS, Id: R01 CA136673
  • Agency: NCI NIH HHS, Id: R01CA120979
  • Agency: NIDDK NIH HHS, Id: R01DK060758
  • Agency: NHLBI NIH HHS, Id: T35 HL007616
  • Agency: NCI NIH HHS, Id: U54 CA126513
  • Agency: NCI NIH HHS, Id: U54 CA126513-05
  • Agency: NCI NIH HHS, Id: U54 CA163004
  • Agency: NCI NIH HHS, Id: U54 CA163004-02

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