{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["44(1)"],"submitter":["Cencioni C"],"pubmed_abstract":["<h4>Background</h4>Metabolic syndrome represents a pancreatic ductal adenocarcinoma (PDAC) risk factor. Metabolic alterations favor PDAC onset, which occurs early upon dysmetabolism. Pancreatic neoplastic lesions evolve within a dense desmoplastic stroma, consisting in abundant extracellular matrix settled by cancer associated fibroblasts (CAFs). Hereby, dysmetabolism and PDAC association was analyzed focusing on CAF functions.<h4>Methods</h4>PDAC development upon dysmetabolic conditions was investigated in: 1) high fat diet fed wild type immunocompetent syngeneic mice by orthotopic transplantation of pancreatic intraepithelial neoplasia (PanIN) organoids; and 2) primary pancreatic CAFs isolated from chemotherapy naïve PDAC patients with/without an history of metabolic syndrome.<h4>Results"],"journal":["Journal of experimental & clinical cancer research : CR"],"pagination":["18"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11744909"],"repository":["biostudies-literature"],"pubmed_title":["The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen proline hydroxylation and favoring T lymphocyte infiltration."],"pmcid":["PMC11744909"],"pubmed_authors":["Bartolazzi A","Cencioni C","Spallotta F","Kunkl M","Tortora G","Corbo V","Ranieri D","Agostini A","Vigiano Benedetti V","Conte F","Larghi A","Licursi V","Carbone C","Perfetto L","Malatesta S","Tuosto L","Piro G"],"additional_accession":[]},"is_claimable":false,"name":"The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen proline hydroxylation and favoring T lymphocyte infiltration.","description":"<h4>Background</h4>Metabolic syndrome represents a pancreatic ductal adenocarcinoma (PDAC) risk factor. Metabolic alterations favor PDAC onset, which occurs early upon dysmetabolism. Pancreatic neoplastic lesions evolve within a dense desmoplastic stroma, consisting in abundant extracellular matrix settled by cancer associated fibroblasts (CAFs). Hereby, dysmetabolism and PDAC association was analyzed focusing on CAF functions.<h4>Methods</h4>PDAC development upon dysmetabolic conditions was investigated in: 1) high fat diet fed wild type immunocompetent syngeneic mice by orthotopic transplantation of pancreatic intraepithelial neoplasia (PanIN) organoids; and 2) primary pancreatic CAFs isolated from chemotherapy naïve PDAC patients with/without an history of metabolic syndrome.<h4>Results","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-01T20:42:41.289Z","creation":"2026-05-21T03:08:42.751Z"},"accession":"S-EPMC11744909","cross_references":{"pubmed":["39828692"],"doi":["10.1186/s13046-024-03263-w"]}}