| First Author | Quante M | Year | 2012 |
| Journal | Cancer Cell | Volume | 21 |
| Issue | 1 | Pages | 36-51 |
| PubMed ID | 22264787 | Mgi Jnum | J:180282 |
| Mgi Id | MGI:5306057 | Doi | 10.1016/j.ccr.2011.12.004 |
| Citation | Quante M, et al. (2012) Bile Acid and inflammation activate gastric cardia stem cells in a mouse model of barrett-like metaplasia. Cancer Cell 21(1):36-51 |
| abstractText | 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-1beta 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-1beta-IL-6 signaling cascade and Dll1-dependent Notch signaling. |
