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GLUTAMINE METABOLISM AND ITS INHIBITION IN THE TARGETING OF STEM CELLS OF CHRONIC MYELOID LEUKAEMIA REFRACTORY TO STANDARD THERAPY
Vol 32, Issue 4S1, 2018
Abstract
We previously found that the adaptation of Chronic Myeloid Leukaemia (CML) cells to energyrestrictions in paralleled by the suppression of BCR/Ablprotein, the oncogenic driver of CML,notably in a subset of leukaemia stem cells (LSC). These LSC, while remaining genetically leukaemic,are independent of BCR/Abl signaling for maintenance in tissues (within the “stem cell niches”) andtherefore refractory to tyrosine kinase inhibitors (TKi) used for CML therapy. We envisioned on thesebases a “metabolic” stem cell niche model to explain the long-term persistence of LSC responsible forMinimal Residual Disease (MRD) of CML. In this model, glutamine plays an important role.
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Supporting Agencies
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Medical Genetics, University of Torino Medical School, Italy
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy