2026-06-14T05:17:38Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/132062024-09-27T10:05:44Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19607

00925njm 22002777a 4500 dc Forte, Dorian author Garcia-Fernandez, Maria author Sanchez-Aguilera, Abel author Stavropoulou, Vaia author Fielding, Claire author Martin-Perez, Daniel author Lopez, Juan Antonio author Costa, Ana S H author Tronci, Laura author Nikitopoulou, Efterpi author Barber, Michael author Gallipoli, Paolo author Marando, Ludovica author Fernandez de Castillejo, Carlos Lopez author Tzankov, Alexandar author Dietmann, Sabine author Cavo, Michele author Catani, Lucia author Curti, Antonio author Vazquez, Jesus author Frezza, Christian author Huntly, Brian J author Schwaller, Juerg author Mendez-Ferrer, Simon author 2020-11 Like normal hematopoietic stem cells, leukemic stem cells depend on their bone marrow (BM) microenvironment for survival, but the underlying mechanisms remain largely unknown. We have studied the contribution of nestin+ BM mesenchymal stem cells (BMSCs) to MLL-AF9-driven acute myeloid leukemia (AML) development and chemoresistance in vivo. Unlike bulk stroma, nestin+ BMSC numbers are not reduced in AML, but their function changes to support AML cells, at the expense of non-mutated hematopoietic stem cells (HSCs). Nestin+ cell depletion delays leukemogenesis in primary AML mice and selectively decreases AML, but not normal, cells in chimeric mice. Nestin+ BMSCs support survival and chemotherapy relapse of AML through increased oxidative phosphorylation, tricarboxylic acid (TCA) cycle activity, and glutathione (GSH)-mediated antioxidant defense. Therefore, AML cells co-opt energy sources and antioxidant defense mechanisms from BMSCs to survive chemotherapy. Cell Metab. 2020; 32(5):829-843 10.1016/j.cmet.2020.09.001 1932-7420 Cell metabolism 32966766 http://hdl.handle.net/20.500.12105/13206 Bone Marrow Mesenchymal Stem Cells Support Acute Myeloid Leukemia Bioenergetics and Enhance Antioxidant Defense and Escape from Chemotherapy.