{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bong YS"],"funding":["NCATS NIH HHS","NCI NIH HHS"],"pagination":["80508-80520"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5348337"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(49)"],"pubmed_abstract":["Vitamin D is implicated in the etiology of cancers of the gastrointestinal tract, usually characterized by alteration in the APC/β-catenin/TCF tumor suppressor pathway. The vitamin D receptor (VDR) is also implicated in cardiovascular and skin diseases as well as in immunity. Activated VDR can indirectly alter β-catenin nuclear localization and directly suppress β-catenin/TCF mediated transcriptional activity. We treated VDR null mice with the carcinogen azoxymethane (AOM) and generated mice bearing a mutated APC (hypomorph) on a VDR null background (Apc1638N/+Vdr-/-). VDR null mice do not develop GI or extra-colonic tumors but loss of VDR decreased intestinal tumor latency and increased progression to adenocarcinoma in both models. AOM treatment of VDR null mice also caused squamous cell "],"journal":["Oncotarget"],"pubmed_title":["A role for the vitamin D pathway in non-intestinal lesions in genetic and carcinogen models of colorectal cancer and in familial adenomatous polyposis."],"pmcid":["PMC5348337"],"funding_grant_id":["UL1 TR001409","UL1 TR000101","P30 CA051008","R01 CA129813","P01 CA130821","R21 CA156188"],"pubmed_authors":["Byers SW","Neklason DW","Ahn J","Bong YS","Assefnia S","Bueno De Mesquita PJ","Tuohy T","Burt RW"],"additional_accession":[]},"is_claimable":false,"name":"A role for the vitamin D pathway in non-intestinal lesions in genetic and carcinogen models of colorectal cancer and in familial adenomatous polyposis.","description":"Vitamin D is implicated in the etiology of cancers of the gastrointestinal tract, usually characterized by alteration in the APC/β-catenin/TCF tumor suppressor pathway. The vitamin D receptor (VDR) is also implicated in cardiovascular and skin diseases as well as in immunity. Activated VDR can indirectly alter β-catenin nuclear localization and directly suppress β-catenin/TCF mediated transcriptional activity. We treated VDR null mice with the carcinogen azoxymethane (AOM) and generated mice bearing a mutated APC (hypomorph) on a VDR null background (Apc1638N/+Vdr-/-). VDR null mice do not develop GI or extra-colonic tumors but loss of VDR decreased intestinal tumor latency and increased progression to adenocarcinoma in both models. AOM treatment of VDR null mice also caused squamous cell ","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Dec","modification":"2026-05-30T10:33:49.344Z","creation":"2019-03-27T02:38:34Z"},"accession":"S-EPMC5348337","cross_references":{"pubmed":["27768599"],"doi":["10.18632/oncotarget.12768"]}}