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Nature, ISSN 0028-0836, 03/2015, Volume 519, Issue 7541, pp. 102 - 105
The BCR-ABL1 fusion gene is a driver oncogene in chronic myeloid leukaemia and 30-50% of cases of adult acute lymphoblastic leukaemia(1). Introduction of ABL1... 
CELLS | PONATINIB | MECHANISM | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | RESISTANCE | FOLLOW-UP | PATIENTS RECEIVING IMATINIB | BCR-ABL INHIBITOR | CHRONIC MYELOID-LEUKEMIA | T315I MUTANT | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Molecular Conformation | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors | Protein Kinase Inhibitors - chemistry | Angiogenesis Inhibitors - therapeutic use | Imidazoles - therapeutic use | Phosphorylation - drug effects | Fusion Proteins, bcr-abl - chemistry | Cell Line | Proto-Oncogene Proteins c-abl - genetics | Indazoles - chemistry | Crystallization | Proto-Oncogene Proteins c-abl - chemistry | Angiogenesis Inhibitors - pharmacology | Models, Molecular | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Imidazoles - pharmacology | Drug Repositioning | Indazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Fusion Proteins, bcr-abl - genetics | Vascular Endothelial Growth Factor Receptor-2 - chemistry | Protein Kinase Inhibitors - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Protein Binding | Proto-Oncogene Proteins c-abl - metabolism | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Kidney Neoplasms - drug therapy | Fusion Proteins, bcr-abl - metabolism | Indazoles - therapeutic use | Angiogenesis Inhibitors - chemistry | Drug Screening Assays, Antitumor | Axitinib | Genetic aspects | Research | Gene mutations | Drug resistance | Analysis | Phosphorylation | Inhibitor drugs | Leukemia | Bone marrow | Mutation | Kinases | Drug dosages | Patients | Index Medicus
Journal Article
Lancet Oncology, The, ISSN 1470-2045, 2010, Volume 11, Issue 11, pp. 1029 - 1035
Journal Article
Journal Article
Nature, ISSN 0028-0836, 01/2010, Volume 463, Issue 7280, pp. 501 - 506
In an effort to find new pharmacological modalities to overcome resistance to ATP-binding-site inhibitors of Bcr-Abl, we recently reported the discovery of... 
CELL LUNG-CANCER | KINASE-INHIBITOR | SELECTIVE INHIBITOR | C-ABL | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | DYNAMICS | MUTATIONS | LYMPHOBLASTIC-LEUKEMIA | IMATINIB RESISTANCE | CHRONIC MYELOID-LEUKEMIA | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Male | Transplantation, Heterologous | Piperazines - chemistry | Pyrimidines - chemistry | Pyrimidines - metabolism | Antineoplastic Agents - metabolism | Mass Spectrometry | Bone Marrow Transplantation | Inhibitory Concentration 50 | Female | Antineoplastic Agents - pharmacology | Binding Sites | Disease Models, Animal | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Protein Structure, Tertiary | Crystallization | Antineoplastic Combined Chemotherapy Protocols | Models, Molecular | Pyrimidines - pharmacology | Antineoplastic Agents - chemistry | Mutation - genetics | Imatinib Mesylate | Piperazines - pharmacology | Fusion Proteins, bcr-abl - genetics | Animals | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice | Benzamides | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Nilotinib | Dasatinib | Drug resistance in microorganisms | Usage | Nuclear magnetic resonance spectroscopy | Research | Chronic myeloid leukemia | X-ray crystallography | Chromosome abnormalities | Gene mutations | Analysis | Genetic aspects | Diagnosis | Binding proteins | Drug therapy | Health aspects | Proteins | Studies | Competition | Enzymes | E coli | Kinases | Drug resistance | Crystal structure | Index Medicus
Journal Article
by Guo, G and Kang, Q and Zhu, X and Chen, Q and Wang, X and Chen, Y and Ouyang, J and Zhang, L and Tan, H and Chen, R and Huang, S and Chen, J.-L
Oncogene, ISSN 0950-9232, 04/2015, Volume 34, Issue 14, pp. 1768 - 1779
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
Nature, ISSN 0028-0836, 08/2010, Volume 466, Issue 7307, pp. 765 - 768
Chronic myelogenous leukaemia (CML) can progress from a slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this... 
CHRONIC MYELOGENOUS LEUKEMIA | MURINE MODEL | STEM-CELLS | TRANSLATIONAL REPRESSION | RNA | BINDING PROTEIN MUSASHI-1 | MULTIDISCIPLINARY SCIENCES | BCR-ABL | GENE-EXPRESSION | NUMB | CML BLAST CRISIS | RNA-Binding Proteins - genetics | Up-Regulation | Oncogene Proteins, Fusion - metabolism | Prognosis | Homeodomain Proteins - metabolism | Humans | Gene Expression Regulation, Neoplastic | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Nuclear Pore Complex Proteins - genetics | Cell Differentiation - genetics | RNA-Binding Proteins - biosynthesis | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Nerve Tissue Proteins - biosynthesis | Membrane Proteins - metabolism | Blast Crisis - pathology | Signal Transduction | Membrane Proteins - genetics | Nuclear Pore Complex Proteins - metabolism | Mice, Inbred C57BL | Tumor Suppressor Protein p53 - metabolism | Receptor, Notch1 - metabolism | Nerve Tissue Proteins - genetics | Disease Progression | Homeodomain Proteins - genetics | Nerve Tissue Proteins - metabolism | Fusion Proteins, bcr-abl - genetics | Membrane Proteins - biosynthesis | Animals | Oncogene Proteins, Fusion - genetics | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Blast Crisis - genetics | Mice | Blast Crisis - metabolism | Fusion Proteins, bcr-abl - metabolism | RNA-Binding Proteins - metabolism | Myelocytic leukemia | Molecular genetics | Physiological aspects | Development and progression | Nonlymphoid leukemia | Cellular signal transduction | Genetic aspects | Research | Genetic regulation | Gene expression | Medical research | Stem cells | Chronic illnesses
Journal Article