{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nimmakayala RK"],"funding":["DH | NIHR | Health Services Research Programme","NCI NIH HHS"],"pagination":["215-231"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10041665"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["40(1)"],"pubmed_abstract":["Pancreatic ductal adenocarcinoma (PDAC) metastasizes to distant organs, which is the primary cause of mortality; however, specific features mediating organ-specific metastasis remain unexplored. Emerging evidence demonstrates that cancer stem cells (CSCs) and cellular metabolism play a pivotal role in metastasis. Here we investigated the role of distinct subtypes of pancreatic CSCs and their metabolomic signatures in organ-specific metastatic colonization. We found that PDAC consists of ALDH+/CD133+ and drug-resistant (MDR1+) subtypes of CSCs with specific metabolic and stemness signatures. Human PDAC tissues with gemcitabine treatment, autochthonous mouse tumors from Kras<sup>G12D</sup>; Pdx1-Cre (KC) and Kras<sup>G12D</sup>; Trp53<sup>R172H</sup>; Pdx-1 Cre (KPC) mice, and KPC- Liver/Lun"],"journal":["Oncogene"],"pubmed_title":["Metabolic programming of distinct cancer stem cells promotes metastasis of pancreatic ductal adenocarcinoma."],"pmcid":["PMC10041665"],"funding_grant_id":["R01 CA210637","U01 CA200466","R01 CA195586","R01 CA183459","R01 CA247471","R01 CA201444","U01 CA210240","P01 CA217798","R01 CA228524"],"pubmed_authors":["Gupta R","Rauth S","Shailendra GK","Chirravuri R","Grandgenett PM","Chhonker YS","Ponnusamy MP","Rachagani S","Nimmakayala RK","Mallya K","Leon F","L Grem J","Murry DJ","Marimuthu S","Hollingsworth MA","Prajapati DR","Lele SM","C Caffrey T","Batra SK","Nallasamy P","Chugh S"],"additional_accession":[]},"is_claimable":false,"name":"Metabolic programming of distinct cancer stem cells promotes metastasis of pancreatic ductal adenocarcinoma.","description":"Pancreatic ductal adenocarcinoma (PDAC) metastasizes to distant organs, which is the primary cause of mortality; however, specific features mediating organ-specific metastasis remain unexplored. Emerging evidence demonstrates that cancer stem cells (CSCs) and cellular metabolism play a pivotal role in metastasis. Here we investigated the role of distinct subtypes of pancreatic CSCs and their metabolomic signatures in organ-specific metastatic colonization. We found that PDAC consists of ALDH+/CD133+ and drug-resistant (MDR1+) subtypes of CSCs with specific metabolic and stemness signatures. Human PDAC tissues with gemcitabine treatment, autochthonous mouse tumors from Kras<sup>G12D</sup>; Pdx1-Cre (KC) and Kras<sup>G12D</sup>; Trp53<sup>R172H</sup>; Pdx-1 Cre (KPC) mice, and KPC- Liver/Lun","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jan","modification":"2025-04-04T20:20:36.259Z","creation":"2025-04-04T20:20:36.259Z"},"accession":"S-EPMC10041665","cross_references":{"pubmed":["33110235"],"doi":["10.1038/s41388-020-01518-2"]}}