{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Quante M"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS","NCI NIH HHS"],"pagination":["36-51"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3266546"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["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"],"journal":["Cancer cell"],"pubmed_title":["Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett-like metaplasia."],"pmcid":["PMC3266546"],"funding_grant_id":["T35 HL007616","U54 CA126513","R01 DK060758","K07 CA132892","R01CA120979","U01 CA143056","R01 CA136673","R01 CA120979","5U01 CA143056","U54 CA163004","R01DK060758","1U54CA126513,","P30-DK050306","P01-CA098101","P30 DK050306","P01 CA098101"],"pubmed_authors":["Friedman R","Lee MD","Dubeykovskaya Z","Rustgi AK","Shawber C","Quante M","Wang TC","Bhagat G","Marache F","Abrams JA","Good P","Asfaha S","Lightdale CJ","Lee Y","Figueiredo JL","Kitajewski J","Mahmood U"],"additional_accession":[]},"is_claimable":false,"name":"Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett-like metaplasia.","description":"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","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jan","modification":"2026-04-30T19:02:29.16Z","creation":"2019-03-27T00:48:27Z"},"accession":"S-EPMC3266546","cross_references":{"pubmed":["22264787"],"doi":["10.1016/j.ccr.2011.12.004"]}}