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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
Journal Article
Journal Article
Journal Article
Nature Medicine, ISSN 1078-8956, 02/2016, Volume 22, Issue 2, pp. 194 - 201
Journal Article
Cancer Discovery, ISSN 2159-8274, 2014, Volume 4, Issue 7, pp. 816 - 827
Journal Article
Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 129 - 132
The epidermal growth factor receptor (EGFR)-directed tyrosine kinase inhibitors (TKIs) gefitinib, erlotinib and afatinib are approved treatments for non-small... 
CELL LUNG-CANCER | EGFR KINASE | GROWTH-FACTOR RECEPTOR | TARGETED THERAPIES | GEFITINIB | ACTIVATION | MECHANISM | MULTIDISCIPLINARY SCIENCES | MUTATIONS | AZD9291 | Lung Neoplasms - drug therapy | Drug Resistance, Multiple - drug effects | Protein Conformation - drug effects | ErbB Receptors - genetics | Lung Neoplasms - pathology | Antineoplastic Agents - pharmacology | Benzeneacetamides - pharmacology | Mutant Proteins - antagonists & inhibitors | Disease Models, Animal | Allosteric Regulation - drug effects | Carcinoma, Non-Small-Cell Lung - pathology | Drug Resistance, Multiple - genetics | ErbB Receptors - antagonists & inhibitors | ErbB Receptors - metabolism | Lung Neoplasms - enzymology | Allosteric Site - drug effects | Mutant Proteins - genetics | Cetuximab - pharmacology | Mutant Proteins - metabolism | Drug Synergism | Drug Resistance, Neoplasm - genetics | Animals | ErbB Receptors - chemistry | Mutant Proteins - chemistry | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Protein Multimerization - drug effects | Drug Resistance, Neoplasm - drug effects | Studies | Phosphorylation | Nuclear magnetic resonance--NMR | Epidermal growth factor | Mutation | Kinases | Enzyme kinetics | Tumors
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 | MECHANISM | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | KINASE | C-RAF | B-RAF | MUTATIONS | PROTEINS | 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 | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article