2026-06-14T05:06:59Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/132062024-09-27T10:05:44Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19607
Repisalud
author
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
funder
Wellcome Trust
funder
MRC Cambridge Stem Cell Institute
funder
Instituto de Salud Carlos III
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Fundación ProCNIC
funder
Fundación La Marató TV3
funder
Fundación La Caixa
funder
Medical Research Council (Reino Unido)
funder
Swiss National Research Foundation
funder
Gertrude von Meissner Foundation
funder
Comunidad de Madrid (España)
funder
National Health Service Blood and Transplant (Reino Unido)
funder
Cancer Research UK (Reino Unido)
funder
Howard Hughes Medical Institute
2021-06-29T06:59:37Z
2021-06-29T06:59:37Z
2020-11
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
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.
eng
Bone Marrow Mesenchymal Stem Cells Support Acute Myeloid Leukemia Bioenergetics and Enhance Antioxidant Defense and Escape from Chemotherapy.
journal article
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BoneMarrowMesenchymalStem_2020.pdf.txt