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Nature medicine, ISSN 1078-8956, 10/2017, Volume 23, Issue 10, pp. 1234 - 1240
Treatment of chronic myeloid leukemia (CML) with imatinib mesylate and other second/third generation c-Abl specific tyrosine kinase inhibitors (TKIs) has... 
Journal Article
Blood, ISSN 0006-4971, 12/2016, Volume 128, Issue 22, pp. 932 - 932
Abstract We and others have shown that tyrosine kinase inhibitors (TKIs), such as imatinib, fail to eliminate primitive chronic myeloid leukaemia (CML) stem... 
Journal Article
Nature Medicine, ISSN 1078-8956, 10/2017, Volume 23, Issue 10, pp. 1234 - 1240
Treatment of chronic myeloid leukemia (CML) with imatinib mesylate and other second-and/or third-generation c-Abl-specific tyrosine kinase inhibitors (TKIs)... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | KINASE-ACTIVITY | COMPLETE MOLECULAR REMISSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DISCONTINUATION | CELL BIOLOGY | BCR | METABOLISM | FATTY-ACID OXIDATION | IMATINIB | SUPPORTING ASPARTATE BIOSYNTHESIS | DIFFERENTIATION | Metabolomics | Up-Regulation | Minocycline - pharmacology | Neoplastic Stem Cells - drug effects | Humans | Minocycline - analogs & derivatives | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Oxidative Phosphorylation - drug effects | Imatinib Mesylate - therapeutic use | Neoplastic Stem Cells - metabolism | Mass Spectrometry | Chromatography, Liquid | Female | Tumor Cells, Cultured | Drug Therapy, Combination | Cell Survival - drug effects | Tumor Stem Cell Assay | Imatinib Mesylate - pharmacology | Mitochondria - metabolism | Mitochondria - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Phenformin - pharmacology | Hypoglycemic Agents - pharmacology | Xenograft Model Antitumor Assays | Animals | Protein Kinase Inhibitors - therapeutic use | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice, Inbred NOD | Anti-Bacterial Agents - pharmacology | Mice | Protein Kinase Inhibitors - pharmacology | In Vitro Techniques | Drug Resistance, Neoplasm - drug effects | Oxidative stress | Care and treatment | Genotype | Development and progression | Genetic aspects | Chronic myeloid leukemia | Health aspects | Phosphorylation | Transformation | Target recognition | Oxidative metabolism | Leukemia | Xenotransplantation | Disease resistance | Oxidation resistance | Mitochondria | Transformed cells | CD38 antigen | Xenografts | Drug therapy | Protein-tyrosine kinase | Chronic illnesses | Tyrosine | CD34 antigen | Imatinib | Cell survival | Myeloid leukemia | Minimal residual disease | Metabolism | Survival | Oxidative phosphorylation | Antibiotics | Stem cells | Tigecycline
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2009, Volume 119, Issue 5, pp. 1109 - 1123
Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | MALIGNANT GLIOMA-CELLS | BLAST CRISIS | CLINICAL RESISTANCE | BCR-ABL MUTATIONS | ENDOPLASMIC-RETICULUM | CYTOCHROME-C RELEASE | CASPASE ACTIVATION | IMATINIB RESISTANCE | CHRONIC MYELOID-LEUKEMIA | Transcription Factor CHOP - genetics | Neoplastic Stem Cells - cytology | Gene Expression - drug effects | Calcium - metabolism | Gene Expression - genetics | Microtubule-Associated Proteins - metabolism | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Endoplasmic Reticulum - metabolism | Antineoplastic Agents - therapeutic use | Autophagy - physiology | Thiazoles - therapeutic use | Autophagy - drug effects | Chloroquine - pharmacology | Neoplastic Stem Cells - metabolism | RNA Interference | Endoplasmic Reticulum - drug effects | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Macrolides - pharmacology | Antineoplastic Agents - pharmacology | Cell Death - drug effects | Dasatinib | Chloroquine - therapeutic use | Piperazines - therapeutic use | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Mice, Inbred C3H | Xenograft Model Antitumor Assays | Fusion Proteins, bcr-abl - genetics | Animals | Cell Death - physiology | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Benzamides | Macrolides - therapeutic use | Protein-Tyrosine Kinases - antagonists & inhibitors | Causes of | Physiological aspects | Genetic aspects | Chronic myeloid leukemia | Research | Drug therapy | Phagocytosis
Journal Article
Frontiers in Cell and Developmental Biology, ISSN 2296-634X, 09/2018, Volume 6, p. 120
Journal Article
Blood, ISSN 0006-4971, 02/2012, Volume 119, Issue 6, pp. 1501 - 1510
Journal Article
Journal Article
Molecular & Cellular Oncology, ISSN 2372-3556, 01/2018, Volume 5, Issue 1, p. e1403532
We have recently uncovered an abnormal increase in mitochondrial oxidative metabolism in therapy-resistant chronic myeloid leukaemia stem cells (LSCs). By... 
Imatinib | CML | Tyrosine kinase inhibitor | TCA cycle | OXPHOS | Cancer stem cells | Metabolism | Tigecycline | Leukaemia
Journal Article
STEM CELLS, ISSN 1066-5099, 09/2014, Volume 32, Issue 9, pp. 2324 - 2337
Chronic myeloid leukemia (CML) is initiated and maintained by the tyrosine kinase BCR‐ABL which activates a number of signal transduction pathways, including... 
FOXO transcription factors | CD34+ progenitor cells | Chronic myeloid leukemia | BCR‐ABL | Tyrosine kinase inhibitors | Quiescence | BCR-ABL | SURVIVAL | APOPTOSIS | STEM-CELLS | CML | PERSISTENCE | CD34(+) progenitor cells | CELL & TISSUE ENGINEERING | CELL BIOLOGY | MAINTENANCE | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | IMATINIB | RESISTANCE | QUIESCENT | HEMATOLOGY | REMISSION | Forkhead Transcription Factors - biosynthesis | Phosphorylation | Signal Transduction | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Gene Expression Profiling | G1 Phase - drug effects | Forkhead Transcription Factors - genetics | Dasatinib - pharmacology | Animals | Transfection | Cell Cycle Checkpoints - drug effects | Forkhead Transcription Factors - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | K562 Cells | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Neoplastic Stem Cells - pathology | Mice | Protein Kinase Inhibitors - pharmacology | Cellular signal transduction | Genetic engineering | DNA binding proteins | Analysis | Stem cells | Transcription factors | Kinases | Leukemia | Rodents | Apoptosis | Cancer Stem Cells
Journal Article
Haematologica, ISSN 0390-6078, 09/2013, Volume 98, Issue 9, pp. 1335 - 1343
Journal Article