<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>44(1)</volume><submitter>Cencioni C</submitter><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pagination>18</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11744909</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen proline hydroxylation and favoring T lymphocyte infiltration.</pubmed_title><pmcid>PMC11744909</pmcid><pubmed_authors>Bartolazzi A</pubmed_authors><pubmed_authors>Cencioni C</pubmed_authors><pubmed_authors>Spallotta F</pubmed_authors><pubmed_authors>Kunkl M</pubmed_authors><pubmed_authors>Tortora G</pubmed_authors><pubmed_authors>Corbo V</pubmed_authors><pubmed_authors>Ranieri D</pubmed_authors><pubmed_authors>Agostini A</pubmed_authors><pubmed_authors>Vigiano Benedetti V</pubmed_authors><pubmed_authors>Conte F</pubmed_authors><pubmed_authors>Larghi A</pubmed_authors><pubmed_authors>Licursi V</pubmed_authors><pubmed_authors>Carbone C</pubmed_authors><pubmed_authors>Perfetto L</pubmed_authors><pubmed_authors>Malatesta S</pubmed_authors><pubmed_authors>Tuosto L</pubmed_authors><pubmed_authors>Piro G</pubmed_authors></additional><is_claimable>false</is_claimable><name>The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen proline hydroxylation and favoring T lymphocyte infiltration.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan</publication><modification>2026-06-01T20:42:41.289Z</modification><creation>2026-05-21T03:08:42.751Z</creation></dates><accession>S-EPMC11744909</accession><cross_references><pubmed>39828692</pubmed><doi>10.1186/s13046-024-03263-w</doi></cross_references></HashMap>