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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
Chemical Biology & Drug Design, ISSN 1747-0277, 01/2011, Volume 77, Issue 1, pp. 1 - 11
The BCR‐ABL inhibitor imatinib has revolutionized the treatment of chronic myeloid leukemia. However, drug resistance caused by kinase domain mutations has... 
kinase | ponatinib | AP24534 | drug discovery | X‐ray crystallography | structure‐based drug design | X-ray crystallography | Structure-based drug design | Drug discovery | Ponatinib | Kinase | structure-based drug design | C-ABL | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | BMS-354825 | DOMAIN MUTATIONS | CANCER | CHRONIC MYELOID-LEUKEMIA | STRATEGIES | THERAPY | IMATINIB | T315I MUTANT | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Piperazines - chemistry | Structure-Activity Relationship | Pyridazines - pharmacology | Pyridazines - chemical synthesis | Pyrimidines - chemistry | Protein Kinase Inhibitors - chemistry | Protein Binding - drug effects | Imidazoles - chemical synthesis | Imidazoles - therapeutic use | Pyridazines - therapeutic use | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Imidazoles - pharmacology | Piperazines - therapeutic use | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Drug Resistance, Neoplasm - genetics | Fusion Proteins, bcr-abl - genetics | Animals | Mutation - drug effects | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Benzamides | Fluoroimmunoassay | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Drug resistance | Analysis | Leukemia | STRUCTURE-ACTIVITY RELATIONSHIPS | MUTANTS | BASIC BIOLOGICAL SCIENCES | ENZYME INHIBITORS | TYROSINE | GENE MUTATIONS | PHOSPHOTRANSFERASES | MYELOID LEUKEMIA | MUTATIONS | ANTINEOPLASTIC DRUGS | 60 APPLIED LIFE SCIENCES | RESIDUES
Journal Article
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 01/2013, Volume 19, Issue 1, pp. 279 - 290
Journal Article
International Journal of Cancer, ISSN 0020-7136, 2014, Volume 134, Issue 6, pp. 1484 - 1494
Crizotinib is an oral tyrosine kinase inhibitor approved for treating patients with non-small cell lung cancer (NSCLC) containing an anaplastic lymphoma kinase... 
brain accumulation | crizotinib | P‐glycoprotein | ALK inhibitor | elacridar | P-glycoprotein | LUNG | EML4-ALK FUSION GENE | METASTASES | PENETRATION | GF120918 | COMBINATION | ANAPLASTIC LYMPHOMA KINASE | PHARMACOKINETICS | ONCOLOGY | MULTIDRUG-RESISTANCE | PHASE-I | ATP Binding Cassette Transporter, Sub-Family G, Member 2 | Humans | ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism | Pyridines - pharmacokinetics | Biological Availability | Male | ATP-Binding Cassette, Sub-Family B, Member 1 - antagonists & inhibitors | Neoplasm Proteins - metabolism | ATP-Binding Cassette Transporters - physiology | Brain - metabolism | Tissue Distribution | ATP-Binding Cassette Transporters - genetics | ATP-Binding Cassette Transporters - metabolism | Drug Therapy, Combination | Neoplasm Proteins - genetics | Pyrazoles - pharmacokinetics | Pyrazoles - pharmacology | Protein Kinase Inhibitors - pharmacokinetics | Tetrahydroisoquinolines - pharmacology | Administration, Oral | Cells, Cultured | Mice, Knockout | Brain - drug effects | Animals | ATP-Binding Cassette, Sub-Family B, Member 1 - genetics | Acridines - pharmacology | ATP Binding Cassette Transporter, Sub-Family B | Mice | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Plasma | Chemotherapy | Brain cancer | Rodents | Lymphomas | Glycoproteins | Metastasis
Journal Article
The Lancet Oncology, ISSN 1470-2045, 06/2018, Volume 19, Issue 6, pp. 747 - 757
Tyrosine kinase inhibitors (TKIs) have improved the survival of patients with chronic myeloid leukaemia. Many patients have deep molecular responses, a... 
SURVIVAL | MAJOR MOLECULAR RESPONSE | TREATMENT-FREE REMISSION | ONCOLOGY | IMATINIB DISCONTINUATION | DISEASE | FOLLOW-UP | DASATINIB | WITHDRAWAL SYNDROME | NILOTINIB | PHASE-2 TRIAL | Predictive Value of Tests | Prospective Studies | Humans | Middle Aged | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Male | Antineoplastic Agents - administration & dosage | Protein Kinase Inhibitors - adverse effects | Time Factors | Antineoplastic Agents - adverse effects | Clinical Decision-Making | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Polymerase Chain Reaction | Adult | Female | Biomarkers, Tumor - antagonists & inhibitors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - mortality | Drug Administration Schedule | Risk Assessment | Europe | Risk Factors | Protein Kinase Inhibitors - administration & dosage | Fusion Proteins, bcr-abl - genetics | Progression-Free Survival | Fusion Proteins, bcr-abl - antagonists & inhibitors | Aged | Biomarkers, Tumor - genetics | Antimitotic agents | Tyrosine | Antineoplastic agents | Analysis | Life Sciences | Hematology | Human health and pathology | Clinical Medicine | Medical and Health Sciences | Cancer and Oncology | Klinisk medicin | Medicin och hälsovetenskap | Cancer och onkologi
Journal Article
Cancer Discovery, ISSN 2159-8274, 04/2017, Volume 7, Issue 4, pp. 400 - 409
Entrectinib, a potent oral inhibitor of the tyrosine kinases TRKA/B/C, ROS1, and ALK, was evaluated in two phase I studies in patients with advanced or... 
REARRANGEMENT | ONCOGENE | ONCOLOGY | ANALOG SECRETORY CARCINOMA | LANDSCAPE | KINASE FUSIONS | SARCOMAS | ETV6-NTRK3 GENE FUSION | CRIZOTINIB | GENOMIC ALTERATIONS | CLINICAL-RESPONSE | Benzamides - pharmacokinetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Receptor, trkA - antagonists & inhibitors | Male | Receptor, trkB - genetics | Indazoles - administration & dosage | Protein Kinase Inhibitors - adverse effects | Mammary Analogue Secretory Carcinoma - genetics | Dose-Response Relationship, Drug | Benzamides - administration & dosage | Membrane Glycoproteins - antagonists & inhibitors | Receptor, trkC - genetics | Anaplastic Lymphoma Kinase | Melanoma - genetics | Colorectal Neoplasms - drug therapy | Receptor, trkB - antagonists & inhibitors | Aged, 80 and over | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Benzamides - adverse effects | Carcinoma, Non-Small-Cell Lung - pathology | Crizotinib | Protein Kinase Inhibitors - pharmacokinetics | Proto-Oncogene Proteins - antagonists & inhibitors | Pyridines - administration & dosage | Carcinoma, Non-Small-Cell Lung - genetics | Receptor, trkC - antagonists & inhibitors | Melanoma - pathology | Mammary Analogue Secretory Carcinoma - drug therapy | Membrane Glycoproteins - genetics | Protein Kinase Inhibitors - administration & dosage | Sequestosome-1 Protein - genetics | Pyrazoles - administration & dosage | Indazoles - pharmacokinetics | Receptor Protein-Tyrosine Kinases - genetics | Oncogene Proteins, Fusion - genetics | Melanoma - drug therapy | Adolescent | Receptor, trkA - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Indazoles - adverse effects | Colorectal Neoplasms - pathology | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Nature, ISSN 0028-0836, 03/2017, Volume 543, Issue 7647, pp. 733 - 737
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 04/2012, Volume 122, Issue 4, pp. 1377 - 1392
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2015, Volume 125, Issue 5, pp. 1780 - 1789
Kinase inhibitors have played an increasingly prominent role in the treatment of cancer and other diseases. Currently, more than 25 oncology drugs that target... 
MEDICINE, RESEARCH & EXPERIMENTAL | ONCOGENIC ACTIVATION | PROTEIN-KINASE | TUMOR-INFILTRATING MACROPHAGES | ADAPTIVE RESISTANCE | ACQUIRED-RESISTANCE | CLINICAL RESISTANCE | DIACYLGLYCEROL KINASES | RECEPTOR TYROSINE KINASE | IMATINIB MESYLATE | ANTITUMOR EFFICACY | Immunotherapy - methods | Apoptosis - drug effects | Humans | Substrate Specificity | Drug Resistance, Neoplasm | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Neoplasms - genetics | Protein Processing, Post-Translational - drug effects | Drug Design | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Molecular Targeted Therapy - methods | Neoplasms - enzymology | Gene Fusion | Enzyme Activation - drug effects | Neoplasms - drug therapy | Drug Synergism | Point Mutation | Gene Amplification | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Oncogene Proteins, Fusion - antagonists & inhibitors | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Apoptosis - physiology | Enzyme inhibitors | Physiological aspects | Research | Drug therapy | Phosphotransferases | Health aspects | Cancer | Proteins | Phosphorylation | Gene amplification | Biology | Regulation | Genomes | Mutation | Metastasis | Kinases | Phosphatase | Tumors | Review
Journal Article