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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, 2014, Volume 509, Issue 7501, pp. 492 - 496
The BRAF kinase is mutated, typically Val 600 -> Glu (V600E), to induce an active oncogenic state in a large fraction of melanomas, thyroid cancers, hairy cell... 
ACTIVATION | MELANOMA | MEK INHIBITION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | RAS ONCOGENESIS | CATALYZED OXIDATION REACTIONS | MUTATIONS | CANCER | BETA-ADRENERGIC RECEPTOR | MASS-SPECTROMETRY | Lung Neoplasms - drug therapy | Mitogen-Activated Protein Kinase Kinases - genetics | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Mitogen-Activated Protein Kinase Kinases - metabolism | Copper - metabolism | Cation Transport Proteins - genetics | Female | Hepatolenticular Degeneration - drug therapy | Indoles - pharmacology | Phosphorylation - drug effects | Cation Transport Proteins - deficiency | Chelating Agents - therapeutic use | Proto-Oncogene Proteins B-raf - metabolism | Disease Models, Animal | Lung Neoplasms - genetics | Copper - pharmacology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Chelating Agents - pharmacology | Drug Repositioning | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Proto-Oncogene Proteins B-raf - genetics | Survival Analysis | Cell Line, Tumor | Mice | Cell Transformation, Neoplastic - drug effects | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Copper in the body | Cellular signal transduction | Growth | Health aspects | Cancer cells | Proteins | Signal transduction | Phosphorylation | Diet | Melanoma | Tumorigenesis | Mutation | Kinases | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 10/2017, Volume 550, Issue 7674, pp. 133 - 136
Targeted BRAF inhibition (BRAFi) and combined BRAF and MEK inhibition (BRAFi and MEKi) therapies have markedly improved the clinical outcomes of patients with... 
METASTATIC MELANOMA | MEK | EPITHELIAL-CELLS | PHOSPHORYLATION | PATHWAY | RAF | P21-ACTIVATED-KINASE-1 | MULTIDISCIPLINARY SCIENCES | KINASE | MECHANISMS | THERAPIES | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | p21-Activated Kinases - antagonists & inhibitors | Melanoma - enzymology | JNK Mitogen-Activated Protein Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Proto-Oncogene Proteins c-raf - chemistry | Female | beta Catenin - chemistry | Phosphorylation - drug effects | p21-Activated Kinases - genetics | JNK Mitogen-Activated Protein Kinases - chemistry | Enzyme Activation - drug effects | p21-Activated Kinases - metabolism | beta Catenin - metabolism | Proto-Oncogene Proteins c-raf - metabolism | Mitogen-Activated Protein Kinase Kinases - chemistry | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Drug Resistance, Neoplasm - drug effects | Melanoma | Physiological aspects | Cellular signal transduction | Drug resistance | Observations | Health aspects | Mitogen-activated protein kinases | TOR protein | Therapy | Phosphorylation | Activation | Metastasis | Drug development | Kinases | Cancer therapies | Metastases | Proteins | β-catenin | Signal transduction | Inhibition | Extracellular signal-regulated kinase | MAP kinase | JNK protein | Patients | Signaling | Protein arrays | Molecular modelling | Biopsy | Cell lines | Apoptosis | 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 Genetics, ISSN 1061-4036, 02/2015, Volume 47, Issue 3, pp. 250 - 256
Resistance to RAF-and MEK-targeted therapy is a major clinical challenge(1-4). RAF and MEK inhibitors are initially but only transiently effective in some but... 
COLON-CANCER | SURVIVAL | LUNG | ACTIVATION | INHIBITION | MELANOMA | SIGNALING PATHWAY | TRANSCRIPTION | GENETICS & HEREDITY | BRAF | KRAS | Humans | Molecular Targeted Therapy | Phosphoproteins - metabolism | Gene Knockdown Techniques | Heterografts | MAP Kinase Signaling System - genetics | HEK293 Cells | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins B-raf - metabolism | MAP Kinase Kinase Kinases - genetics | Protein-Serine-Threonine Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Phosphoproteins - genetics | Mice, SCID | HT29 Cells | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Mice, Inbred NOD | Biomarkers, Tumor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Genes, ras | Antimitotic agents | Gene mutations | Genetic aspects | Research | Antineoplastic agents | Drug resistance | Health aspects | Thyroid cancer | Lung cancer | Colorectal cancer | Melanoma | Kinases | Charitable foundations | Cancer therapies | Design of experiments | Tumors | Index Medicus
Journal Article
Blood, ISSN 0006-4971, 06/2011, Volume 117, Issue 23, pp. 6287 - 6296
B-cell receptor (BCR) signaling is aberrantly activated in chronic lymphocytic leukemia (CLL). Bruton tyrosine kinase (BTK) is essential to BCR signaling and... 
B-CELLS | CLL | FLUDARABINE PLUS CYCLOPHOSPHAMIDE | APOPTOTIC CELL-DEATH | RITUXIMAB | SURVIVAL SIGNALS | LYMPHOMA | DRUG-RESISTANCE | INHIBITOR | HEMATOLOGY | EXPRESSION | T-Lymphocytes - enzymology | Apoptosis - drug effects | Humans | Tumor Necrosis Factor-alpha - genetics | Cell Survival - genetics | Apoptosis - genetics | Male | NF-kappa B - metabolism | Neoplasm Proteins - antagonists & inhibitors | Receptors, Antigen, B-Cell - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Neoplasm Proteins - genetics | Interleukin-6 - metabolism | Cell Survival - drug effects | Drug Screening Assays, Antitumor - methods | Interleukin-6 - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Gene Expression Regulation, Leukemic - drug effects | Pyrimidines - pharmacology | Leukemia, Lymphocytic, Chronic, B-Cell - enzymology | B-Cell Activating Factor - metabolism | CD40 Ligand - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Gene Expression Regulation, Enzymologic - genetics | Cell Line, Tumor | Receptors, Antigen, B-Cell - genetics | Mice | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Mitogen-Activated Protein Kinase 1 - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Gene Expression Regulation, Leukemic - genetics | Protein-Tyrosine Kinases - genetics | CD40 Ligand - metabolism | MAP Kinase Signaling System - genetics | Female | Interleukin-4 - genetics | Protein-Tyrosine Kinases - biosynthesis | Pyrazoles - pharmacology | B-Lymphocytes - enzymology | Neoplasm Proteins - biosynthesis | Interleukin-4 - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | MAP Kinase Signaling System - drug effects | NF-kappa B - genetics | B-Cell Activating Factor - genetics | Cell Proliferation - drug effects | Index Medicus | Abridged Index Medicus | Lymphoid Neoplasia
Journal Article
Nature, ISSN 0028-0836, 08/2016, Volume 537, Issue 7618, pp. 112 - 116
Deregulation of the Ras-mitogen activated protein kinase (MAPK) pathway is an early event in many different cancers and a key driver of resistance to targeted... 
ACTIVATION | PROTEIN | MEK INHIBITION | MECHANISM | KINASE SUPPRESSOR | COMPLEX REVEALS | MULTIDISCIPLINARY SCIENCES | C-ELEGANS | BRAF | GENE ENCODES | SCAFFOLD | Neoplasms - metabolism | ras Proteins - genetics | Humans | Protein Conformation - drug effects | ras Proteins - metabolism | Enzyme Stability - drug effects | raf Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Neoplasms - genetics | Pyrimidinones - pharmacology | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Allosteric Regulation - drug effects | Cell Line | Oncogenes - genetics | raf Kinases - chemistry | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | ras Proteins - antagonists & inhibitors | Models, Molecular | Neoplasms - enzymology | Neoplasms - drug therapy | Mitogen-Activated Protein Kinase Kinases - chemistry | MAP Kinase Signaling System - drug effects | Alleles | Oncogenes - drug effects | Protein Binding | Protein-Serine-Threonine Kinases - chemistry | Mutation | Quinazolines - pharmacology | Protein Multimerization - drug effects | Pyridones - pharmacology | Physiological aspects | Ras genes | Care and treatment | Phosphotransferases | Methods | Cancer | Signal transduction | Phosphorylation | Genes | Ligands | Kinases | Crystal structure | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 05/2013, Volume 497, Issue 7451, pp. 638 - 642
Journal Article
Oncogene, ISSN 0950-9232, 07/2011, Volume 30, Issue 28, pp. 3153 - 3162
Mice with thyroid-specific expression of oncogenic BRAF (Tg-Braf) develop papillary thyroid cancers (PTCs) that are locally invasive and have well-defined foci... 
TGFΒ | BRAF | thyroid | epithelialmesenchymal transition | CELLS | ACTIVATION | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL BIOLOGY | FALSE DISCOVERY RATE | GENE-EXPRESSION DATA |