Autophagy and Mitochondrial Metabolism: Insights into their Role and Therapeutic Potential in Chronic Myeloid Leukaemia

Despite the development of selective BCR-ABL-targeting tyrosine kinase inhibitors (TKIs) transforming the management of chronic myeloid leukaemia (CML), therapy-resistant leukaemic stem cells (LSCs) persist after TKI treatment and present an obstacle to a CML cure. Recently, we and others have made...

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Detalles Bibliográficos
Autores: Baquero Valls, Pablo|||0000-0002-5292-071X, Dawson, Amy, Helgason, Gudmundur Vignir
Tipo de recurso: artículo
Fecha de publicación:2018
País:España
Institución:Universidad de Alcalá (UAH)
Repositorio:e_Buah Biblioteca Digital Universidad de Alcalá
Idioma:inglés
OAI Identifier:oai:ebuah.uah.es:10017/58890
Acceso en línea:http://hdl.handle.net/10017/58890
https://dx.doi.org/10.1038/s41375-018-0252-4
Access Level:acceso abierto
Palabra clave:autophagy
chronic myeloid leukaemia
metabolism
mitochondria
oxidative phosphorylation
therapeutics
Medicina
Medicine
Descripción
Sumario:Despite the development of selective BCR-ABL-targeting tyrosine kinase inhibitors (TKIs) transforming the management of chronic myeloid leukaemia (CML), therapy-resistant leukaemic stem cells (LSCs) persist after TKI treatment and present an obstacle to a CML cure. Recently, we and others have made significant contributions to the field by unravelling survival dependencies in LSCs to work towards the goal of eradicating LSCs in CML patients. In this review, we describe these findings focusing on autophagy and mitochondrial metabolism, which have recently been uncovered as two essential processes for LSCs quiescence and survival respectively. In addition, we discuss the therapeutic potential of autophagy and mitochondrial metabolism inhibition as a strategy to eliminate CML cells in patients where the resistance to TKI is driven by BCR-ABL-independent mechanism(s).