{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Vinado AC"],"funding":["Cancer Research UK","Medical Research Council"],"pagination":["1969-1979"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7614282"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["36(8)"],"pubmed_abstract":["Eradicating leukemia requires a deep understanding of the interaction between leukemic cells and their protective microenvironment. The CXCL12/CXCR4 axis has been postulated as a critical pathway dictating leukemia stem cell (LSC) chemoresistance in AML due to its role in controlling cellular egress from the marrow. Nevertheless, the cellular source of CXCL12 in the acute myeloid leukemia (AML) microenvironment and the mechanism by which CXCL12 exerts its protective role in vivo remain unresolved. Here, we show that CXCL12 produced by Prx1+ mesenchymal cells but not by mature osteolineage cells provide the necessary cues for the maintenance of LSCs in the marrow of an MLL::AF9-induced AML model. Prx1+ cells promote survival of LSCs by modulating energy metabolism and the REDOX balance in L"],"journal":["Leukemia"],"pubmed_title":["The bone marrow niche regulates redox and energy balance in MLL::AF9 leukemia stem cells."],"pmcid":["PMC7614282"],"funding_grant_id":["26670","C355/A26819","C61367/A26670","MC_PC_17230","MR/V005421/1"],"pubmed_authors":["Luck TJ","Guruceaga E","Bullinger L","Lisi-Vega LE","San Martin-Uriz P","Vilas-Zornoza A","Vinado AC","Valera P","Gomez-Cebrian N","Apaolaza I","Calvo IA","Cenzano I","Planes FJ","Romero JP","Puchades-Carrasco L","Pardo-Saganta A","Saez B","Prosper F","Vera L","Mendez-Ferrer S","Ripalda-Cemborain P","Granero-Molto F","Olaverri D","Rifon JJ","Cocera M","Yusuf RZ"],"additional_accession":[]},"is_claimable":false,"name":"The bone marrow niche regulates redox and energy balance in MLL::AF9 leukemia stem cells.","description":"Eradicating leukemia requires a deep understanding of the interaction between leukemic cells and their protective microenvironment. The CXCL12/CXCR4 axis has been postulated as a critical pathway dictating leukemia stem cell (LSC) chemoresistance in AML due to its role in controlling cellular egress from the marrow. Nevertheless, the cellular source of CXCL12 in the acute myeloid leukemia (AML) microenvironment and the mechanism by which CXCL12 exerts its protective role in vivo remain unresolved. Here, we show that CXCL12 produced by Prx1+ mesenchymal cells but not by mature osteolineage cells provide the necessary cues for the maintenance of LSCs in the marrow of an MLL::AF9-induced AML model. Prx1+ cells promote survival of LSCs by modulating energy metabolism and the REDOX balance in L","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2025-04-04T02:25:52.508Z","creation":"2025-02-19T02:22:13.503Z"},"accession":"S-EPMC7614282","cross_references":{"pubmed":["35618797"],"doi":["10.1038/s41375-022-01601-5"]}}