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Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 5, pp. 401 - 412
Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain... 
CHEMBIO | HUMDISEASE | CHRONIC MYELOGENOUS LEUKEMIA | DASATINIB BMS-354825 | MESYLATE | CML | ONCOLOGY | KINASE DOMAIN MUTATIONS | AMN107 | IMATINIB RESISTANCE | NILOTINIB | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Pyridazines - pharmacology | Protein Kinase Inhibitors - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Antineoplastic Agents - pharmacology | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Proto-Oncogene Proteins c-abl - genetics | Cell Growth Processes - drug effects | Proto-Oncogene Proteins c-abl - chemistry | Models, Molecular | Imidazoles - pharmacology | Antineoplastic Agents - chemistry | Mice, SCID | Pyridazines - chemistry | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-abl - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism | Chronic myeloid leukemia | BCR protein | Imatinib | Mutagenesis | Abl protein | Mutation | Fusion protein | Tumors | Index Medicus | imatinib resistance | dasatinib | nilotinib | compound mutation
Journal Article
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
Nature, ISSN 0028-0836, 03/2017, Volume 543, Issue 7647, pp. 733 - 737
Journal Article
Lancet Oncology, The, ISSN 1470-2045, 2011, Volume 12, Issue 9, pp. 841 - 851
Summary Background Nilotinib has shown greater efficacy than imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid... 
Hematology, Oncology and Palliative Medicine | CHRONIC MYELOGENOUS LEUKEMIA | HALF | THERAPY | ONCOLOGY | MOLECULAR RESPONSES | RECOMMENDATIONS | HARMONIZING CURRENT METHODOLOGY | TYROSINE KINASE INHIBITOR | DISCONTINUATION | BCR-ABL TRANSCRIPTS | Piperazines - administration & dosage | Singapore | Protein-Tyrosine Kinases - metabolism | United States | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Antineoplastic Agents - therapeutic use | Antineoplastic Agents - administration & dosage | Protein Kinase Inhibitors - adverse effects | Protein-Tyrosine Kinases - genetics | Time Factors | Antineoplastic Agents - adverse effects | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Brazil | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - mortality | Philadelphia Chromosome | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Drug Administration Schedule | Administration, Oral | Pyrimidines - administration & dosage | Europe | Kaplan-Meier Estimate | Survival Rate | Treatment Outcome | Piperazines - therapeutic use | Imatinib Mesylate | Piperazines - adverse effects | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Fusion Proteins, bcr-abl - genetics | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Pyrimidines - adverse effects | Benzamides | Australia | Fusion Proteins, bcr-abl - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Antimitotic agents | Antineoplastic agents | Product development
Journal Article
Lancet Oncology, The, ISSN 1470-2045, 2010, Volume 11, Issue 11, pp. 1029 - 1035
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 03/2013, Volume 288, Issue 9, pp. 6116 - 6129
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 02/2014, Volume 32, Issue 5, pp. 415 - 423
Purpose Deep molecular response (MR4.5) defines a subgroup of patients with chronic myeloid leukemia (CML) who may stay in unmaintained remission after... 
MESYLATE | INTERFERON-ALPHA | THERAPY | CHRONIC-PHASE | ONCOLOGY | RECOMMENDATIONS | CLINICAL-TRIALS | 800 MG | END-POINTS | EUROPEAN-LEUKEMIANET | CHRONIC MYELOID-LEUKEMIA | Piperazines - administration & dosage | Humans | Middle Aged | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Male | Protein Kinase Inhibitors - adverse effects | Molecular Targeted Therapy | Young Adult | Benzamides - administration & dosage | Time Factors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Aged, 80 and over | Adult | Female | Benzamides - adverse effects | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - mortality | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Pyrimidines - administration & dosage | Risk Factors | Proportional Hazards Models | Treatment Outcome | Imatinib Mesylate | Piperazines - adverse effects | Remission Induction | Cytarabine - administration & dosage | Disease Progression | Interferon-alpha - administration & dosage | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Fusion Proteins, bcr-abl - genetics | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Adolescent | Fusion Proteins, bcr-abl - antagonists & inhibitors | Pyrimidines - adverse effects | Aged | Fusion Proteins, bcr-abl - metabolism
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 02/2014, Volume 32, Issue 5, pp. 424 - 430
Journal Article
Journal Article
Cancer Letters, ISSN 0304-3835, 2015, Volume 360, Issue 2, pp. 245 - 256
Highlights • MiR-424 expression is low in CML cell lines and patient samples at time of diagnosis. • Using bioinformatics we revealed a conserved miR-424... 
Hematology, Oncology and Palliative Medicine | BCR–ABL | Imatinib | miR-424 | CML | Apoptosis | MiR-424 | BCR-ABL | EXPRESSION PROFILES | MIR-16 FAMILY | CHRONIC MYELOID-LEUKEMIA | TYROSINE KINASE INHIBITORS | SMALL INTERFERING RNA | LYMPHOCYTIC-LEUKEMIA | ONCOLOGY | ENDOTHELIAL-CELLS | GENE-EXPRESSION | CYCLE PROGRESSION | MICRORNA EXPRESSION | Apoptosis - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Apoptosis - genetics | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - therapy | Fusion Proteins, bcr-abl - biosynthesis | Transfection | Base Sequence | Antineoplastic Agents - pharmacology | Benzamides - pharmacology | Cell Growth Processes - genetics | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Cell Growth Processes - drug effects | MicroRNAs - administration & dosage | Down-Regulation | MicroRNAs - biosynthesis | Combined Modality Therapy | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Fusion Proteins, bcr-abl - genetics | Fusion Proteins, bcr-abl - antagonists & inhibitors | K562 Cells | HL-60 Cells | MicroRNAs - genetics | HeLa Cells | Fusion Proteins, bcr-abl - metabolism | Antimitotic agents | Antineoplastic agents | Cell growth | Kinases | Leukemia | Cell cycle
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 11/2012, Volume 367, Issue 22, pp. 2075 - 2088
Ponatinib was developed to overcome resistance to the tyrosine kinase inhibitors used to treat leukemias that are positive for the Philadelphia chromosome. In... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, GENERAL & INTERNAL | RESPONSE CRITERIA | KINASE DOMAIN MUTATIONS | DIAGNOSED CHRONIC-PHASE | TYROSINE KINASE | INTERNATIONAL-WORKING-GROUP | FOLLOW-UP | CLINICAL RESISTANCE | BCR-ABL INHIBITOR | CHRONIC MYELOID-LEUKEMIA | Amylases - blood | Lipase - blood | Follow-Up Studies | Humans | Middle Aged | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Imidazoles - administration & dosage | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Drug Resistance, Neoplasm | Male | Structure-Activity Relationship | Antineoplastic Agents - administration & dosage | Dose-Response Relationship, Drug | Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Protein-Tyrosine Kinases - genetics | Antineoplastic Agents - adverse effects | Pyridazines - administration & dosage | Aged, 80 and over | Adult | Female | Pyridazines - adverse effects | Imidazoles - adverse effects | Antineoplastic Agents - chemistry | Pancreatitis - chemically induced | Pyridazines - chemistry | Fusion Proteins, bcr-abl - genetics | Fusion Proteins, bcr-abl - antagonists & inhibitors | Aged | Mutation | Protein-Tyrosine Kinases - antagonists & inhibitors | Patient outcomes | BCR-ABL tyrosine kinase inhibitors | Dosage and administration | Genetic aspects | Acute lymphocytic leukemia | Research | Drug therapy | Tyrosine | BCR protein | Acute lymphatic leukemia | Myeloid leukemia | Leukemia | Pancreatitis | Abl protein | Chronic myeloid leukemia | Lymphatic leukemia | Lipase | Kinases | Philadelphia chromosome | Proteins | Myelosuppression | Fusion protein | Protein-tyrosine kinase | Binding sites | Index Medicus | Abridged Index Medicus
Journal Article