{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Abdel Hadi N"],"funding":["Fondation ARC pour la Recherche sur le Cancer (ARC Foundation for Cancer Research)"],"pagination":["48"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12690124"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Pancreatic Ductal Adenocarcinoma (PDAC) remains a major unresolved disease because of its remarkable therapeutic resistance. Even patients who respond to initial therapy experience relapse in most cases. The mechanisms underlying therapy-acquired resistance supporting relapse are poorly understood. In this study, we aimed to determine the metabolic features of PDAC during relapse, specifically adaptations of mitochondrial oxidative metabolism. We used preclinical PDAC mouse models (patient-derived xenografts and murine syngeneic allografts) that present regression under initial chemotherapeutic treatment but relapse after a certain time. Relapsed tumors were analyzed ex vivo by flow cytometry to measure mitochondrial and redox characteristics. Molecular mechanisms were investigated by quan"],"journal":["Oncogenesis"],"pubmed_title":["Adaptation of redox metabolism in drug-tolerant persister cells is a vulnerability to prevent relapse in pancreatic cancer."],"pmcid":["PMC12690124"],"funding_grant_id":["PJA20181208207"],"pubmed_authors":["Abdel Hadi N","Gicquel T","Sarry JE","Masoud R","Iovanna J","Gallardo-Arriaga S","Carrier A","Boet E","Cosialls E","Reyes-Castellanos G"],"additional_accession":[]},"is_claimable":false,"name":"Adaptation of redox metabolism in drug-tolerant persister cells is a vulnerability to prevent relapse in pancreatic cancer.","description":"Pancreatic Ductal Adenocarcinoma (PDAC) remains a major unresolved disease because of its remarkable therapeutic resistance. Even patients who respond to initial therapy experience relapse in most cases. The mechanisms underlying therapy-acquired resistance supporting relapse are poorly understood. In this study, we aimed to determine the metabolic features of PDAC during relapse, specifically adaptations of mitochondrial oxidative metabolism. We used preclinical PDAC mouse models (patient-derived xenografts and murine syngeneic allografts) that present regression under initial chemotherapeutic treatment but relapse after a certain time. Relapsed tumors were analyzed ex vivo by flow cytometry to measure mitochondrial and redox characteristics. Molecular mechanisms were investigated by quan","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-07-15T09:15:33.983Z","creation":"2026-07-02T03:08:50.986Z"},"accession":"S-EPMC12690124","cross_references":{"pubmed":["41365870"],"doi":["10.1038/s41389-025-00591-0"]}}