NUMB inactivation confers resistance to imatinib in chronic myeloid leukemia cells

Highlights • NUMB-NOTCH pathway has been involved in progression of CML into blast crisis • NUMB inhibition makes CML cells highly proliferative and imatinib-resistant. • Loss of NUMB function could be an underliyng cause of CML progression and resistance to treatment

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Bibliographische Detailangaben
Veröffentlicht in:	Cancer letters 2016-05, Vol.375 (1), p.92-99
Hauptverfasser:	Garcia-Alegría, Eva, Lafita-Navarro, M. Carmen, Aguado, Rocío, Garcia-Gutierrez, Lucia, Sarnataro, Kyle, Ruiz-Herguido, Cristina, Martín, Francisco, Bigas, Anna, Canelles, Matilde, León, Javier
Format:	Artikel
Sprache:	eng
Schlagworte:	Antineoplastic Agents - pharmacology Cell cycle Cell division Cell Proliferation Chronic myeloid leukemia Cloning Drug Resistance, Neoplasm Flow cytometry Fusion Proteins, bcr-abl - metabolism Gene Expression Genes, Dominant HeLa Cells Hematology, Oncology and Palliative Medicine Humans Imatinib Imatinib Mesylate - pharmacology K562 Cells Kinases Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Membrane Proteins - genetics Membrane Proteins - metabolism Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism NUMB Plasmids Proteins Rodents Signal Transduction Stem cells
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Beschreibung
Zusammenfassung:	Highlights • NUMB-NOTCH pathway has been involved in progression of CML into blast crisis • NUMB inhibition makes CML cells highly proliferative and imatinib-resistant. • Loss of NUMB function could be an underliyng cause of CML progression and resistance to treatment
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2016.02.037