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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 | Index Medicus | Abridged Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 431 - 435
Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | C-RAF | HETERODIMERIZATION | B-RAF | PROTEIN-KINASE KINASE | CANCER | Neoplasms - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Diphenylamine - pharmacology | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | ras Proteins - metabolism | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Adenosine Triphosphate - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Cell Membrane - metabolism | raf Kinases - genetics | Cell Membrane - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Pyrazoles - pharmacology | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Indenes - pharmacology | raf Kinases - chemistry | Proto-Oncogene Proteins c-raf - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins c-raf - deficiency | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Ras genes | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Mitogen-activated protein kinases | Competition | Clinical trials | Enzymes | Kinases | Index Medicus | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 427 - 430
Tumours with mutant BRAF are dependent on the RAF–MEK–ERK signalling pathway for their growth. We found that ATP-competitive RAF inhibitors inhibit ERK... 
SELECTIVE INHIBITOR | ACTIVATION | MELANOMA | MECHANISM | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | HETERODIMERIZATION | KINASE INHIBITOR | B-RAF | CRAF | ONCOGENIC BRAF | Neoplasms - metabolism | ras Proteins - genetics | Phosphorylation | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | Transcriptional Activation - drug effects | ras Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Neoplasms - genetics | Adenosine Triphosphate - metabolism | Indoles - pharmacology | raf Kinases - genetics | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Cell Line | raf Kinases - chemistry | Catalytic Domain | Neoplasms - enzymology | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Models, Biological | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Protein Binding | Mice | Protein Kinase Inhibitors - pharmacology | Protein Kinase Inhibitors - metabolism | Care and treatment | Enzyme inhibitors | Gene mutations | Cellular signal transduction | Genetic aspects | Research | Health aspects | Cancer | Proteins | Competition | Drugs | Mutation | Kinases | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 07/2012, Volume 487, Issue 7408, pp. 505 - 509
Mutationally activated kinases define a clinically validated class of targets for cancer drug therapy(1). However, the efficacy of kinase inhibitors in... 
CELL LUNG-CANCER | SURVIVAL | HETEROGENEITY | ACTIVATION | RECEPTOR TYROSINE KINASES | THERAPY | MET AMPLIFICATION | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | SENSITIVITY | TUMOR-CELLS | Receptor, ErbB-2 - genetics | Humans | Receptor, ErbB-2 - metabolism | Melanoma - enzymology | Phosphatidylinositol 3-Kinases - metabolism | Hepatocyte Growth Factor - pharmacology | Breast Neoplasms - metabolism | Melanoma - genetics | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Cell Survival - drug effects | Melanoma - pathology | Receptor Protein-Tyrosine Kinases - metabolism | Sulfonamides - pharmacology | Breast Neoplasms - drug therapy | Hepatocyte Growth Factor - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Breast Neoplasms - genetics | Signal Transduction - drug effects | Breast Neoplasms - pathology | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Ligands | Protein Kinase Inhibitors - pharmacology | Quinazolines - pharmacology | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinases - metabolism | Antimitotic agents | Physiological aspects | Antineoplastic agents | Growth factors | Health aspects | Phosphotransferases | Substance abuse treatment | Epidermal growth factor | Rodents | Biomarkers | Breast cancer | Insulin-like growth factors | Kinases | Drug resistance | Tumors | Index Medicus
Journal Article
Nature Chemical Biology, ISSN 1552-4450, 2014, Volume 10, Issue 4, pp. 305 - 312
Journal Article
Biochemical Journal, ISSN 0264-6021, 12/2007, Volume 408, Issue 3, pp. 297 - 315
The specificities of 65 compounds reported to be relatively specific inhibitors of protein kinases have been profiled against a panel of 70-80 protein kinases.... 
Drug discovery | Kinase profiling | Protein kinase | Anti-cancer drugs | Inhibitor specificity | RHO-ASSOCIATED KINASE | TUMOR PROGRESSION | FAMILY-MEMBERS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-PROLIFERATION | protein kinase | P38 MAP KINASE | CYCLIN-DEPENDENT KINASES | RECEPTOR TYROSINE KINASES | drug discovery | kinase profiling | SB 203580 | anti-cancer drugs | ISOFORMS IN-VITRO | P90 RSK | inhibitor specificity | Amino Acid Sequence | Cell Line | Phosphorylation | Recombinant Proteins - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Humans | Drug Design | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Mitogen-Activated Protein Kinases - metabolism | Spodoptera | Index Medicus | Yes1, Yamaguchi sarcoma viral oncogene homologue 1 | CSK, C-terminal Src kinase | Lck, lymphocyte cell-specific protein-tyrosine kinase | EGF, epidermal growth factor | FGF-R, fibroblast-growth-factor receptor | PAK, p21-activated protein kinase | PDK, 3-phosphoinositide-dependent protein kinase | PI3K, phosphatidylinositol (phosphoinositide) 3-kinase | NEK, NIMA (never in mitosis in Aspergillus nidulans)-related kinase | RSK, p90 ribosomal S6 kinase | HEK-293 cells, human embryonic kidney-293 cells | VEGF, vascular endothelial growth factor (vasoendothelial growth factor) | EF2K, elongation-factor-2 kinase | CK, casein kinase | PTEN, phosphatase and tensin homologue deleted on chromosome 10 | ERK, extracellular-signal-regulated kinase | ATM, ataxia telangiectasia mutated | SRPK, serine-arginine protein kinase | IL-1, interleukin 1 | MNK, MAPK-integrating protein kinase | ROCK, Rho-dependent protein kinase | CaMKK, CaMK kinase | GST, glutathione transferase | MKK1, MAPK kinase-1 (also called MEK1, MAPK or ERK kinase 1) | GAK, cyclin G-associated kinase | FMK, fluoromethylketone | MST, mammalian homologue Ste20-like kinase | PKA, cAMP-dependent protein kinase | FKBP, FK506-binding protein | PPAR, peroxisome-proliferator-activated receptor | IKK, inhibitory κB kinase | PH, pleckstrin homology | MBP, myelin basic protein | AICAR, aminoimidazole-4-carboxamide-1-β-D-ribofuranoside | MAPKAP-K, MAPK-activated protein kinase | Sf21, Spodoptera frugiperda (fall armyworm) 21 | MARK, microtubule-affinity-regulating kinase | PIM, provirus integration site for Moloney murine leukaemia virus | LPS, lipopolysaccharide | MSK, mitogen- and stress-activated protein kinase | MAPK, mitogen-activated protein kinase | MELK, maternal embryonic leucine-zipper kinase | His6, hexahistidine | CAK, cyclin-dependent kinase-activating kinase | Eph-A2, Ephrin A2 receptor | PLK, polo-like kinase | ATF2, activating transcription factor 2 | PKD, protein kinase D | Src, sarcoma kinase | AMPK, AMP-activated protein kinase | MMS, methyl methanesulfonate | CHK, checkpoint kinase | JNK, c-Jun N-terminal kinase | TORC1, mTOR (mammalian target of rapamycin)–raptor (regulatory associated protein of mTOR) complex | BRSK, brain-specific kinase | RIP2, receptor-interacting protein 2 | IGF-1, insulin-like growth factor-1 | S6K1, S6 kinase 1 | DYRK, dual-specificity tyrosine-phosphorylated and -regulated kinase | HIPK, homeodomain-interacting protein kinase | ZMP, aminoimidazole-4-carboxamide-1-β-D-ribofuranoside monophosphate | PRAK, p38-regulated activated kinase | PKC, protein kinase C | Src-I1, Src inhibitor 1 | TANK, TRAF (tumour-necrosis-factor-receptor-associated factor)-family-member-associated nuclear factor κB activator | NFAT, nuclear factor for activated T-cells | PHK, phosphorylase kinase | GSK3, glycogen synthase kinase 3 | PKB, protein kinase B (also called Akt) | CaMK, calmodulin-dependent kinase | CDK, cyclin-dependent protein kinase | NDRG, N-myc downstream-regulated gene | SmMLCK, smooth-muscle myosin light-chain kinase | TBK1, TANK-binding kinase 1 | PRK, protein kinase C-related kinase | SGK, serum- and glucocorticoid-induced kinase
Journal Article