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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
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, 12/2010, Volume 468, Issue 7326, pp. 968 - 972
Oncogenic mutations in the serine/threonine kinase B-RAF (also known as BRAF) are found in 50-70% of malignant melanomas. Pre-clinical studies have... 
TRANSFORMATION | CELLS | TUMOR PROGRESSION | GENE | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | BRAF | B-RAF | KAPPA-B | MUTATIONS | CANCER | Allosteric Regulation | Humans | Gene Expression Regulation, Neoplastic | Melanoma - enzymology | Gene Expression Profiling | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Indoles - pharmacology | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Gene Library | Proto-Oncogene Proteins c-raf - genetics | MAP Kinase Kinase Kinases - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - genetics | Clinical Trials as Topic | MAP Kinase Kinase Kinases - metabolism | Enzyme Activation - drug effects | Open Reading Frames - genetics | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Indoles - therapeutic use | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinases - metabolism | Protein research | Research | Properties | Protein kinases | Cancer cells | Cell lines | Biochemistry | Mutation | Kinases | Genes | Cancer | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 508, Issue 1, pp. 118 - 122
Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably(1,2).... 
GROWTH-FACTOR RECEPTOR | BRAF INHIBITOR | RAF INHIBITION | CELLS | MULTIDISCIPLINARY SCIENCES | IMPROVED SURVIVAL | DIFFERENTIATION | C-JUN | CANCER | EXPRESSION | EGFR | Receptor, Epidermal Growth Factor - genetics | Humans | Receptor Protein-Tyrosine Kinases - biosynthesis | Cellular Senescence - drug effects | Melanoma - enzymology | Antineoplastic Agents - administration & dosage | Receptor, Platelet-Derived Growth Factor beta - genetics | Indoles - administration & dosage | Mitogen-Activated Protein Kinase Kinases - metabolism | Receptor, Epidermal Growth Factor - metabolism | Flow Cytometry | Melanoma - genetics | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Proto-Oncogene Proteins B-raf - metabolism | Receptor, Platelet-Derived Growth Factor beta - metabolism | Receptor, Epidermal Growth Factor - biosynthesis | Gene Library | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Melanoma - pathology | Receptor Protein-Tyrosine Kinases - metabolism | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Protein Kinase Inhibitors - administration & dosage | Transforming Growth Factor beta - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Receptor Protein-Tyrosine Kinases - genetics | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Transforming Growth Factor beta - metabolism | Receptor, Platelet-Derived Growth Factor beta - biosynthesis | Sulfonamides - administration & dosage | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Proteins | Biopsy | Rodents | Genes | Melanoma | Mutation | Kinases | Drug resistance | Patients | Tumors | Index Medicus
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 04/2012, Volume 18, Issue 8, pp. 2316 - 2325
Purpose: This study evaluated the clinical relevance of the dual-targeting strategy involving PI3K/AKT/mTOR and RAF/MEK/ERK pathways. Experimental Design: We... 
COLON-CANCER | METASTATIC MELANOMA | PIK3CA MUTATIONS | PI3K | ONCOLOGY | COLORECTAL-CANCER | RESISTANCE | BRAF | ANTITUMOR-ACTIVITY | MEK INHIBITORS | TUMORS | Neoplasms - metabolism | Extracellular Signal-Regulated MAP Kinases - drug effects | TOR Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Middle Aged | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | Young Adult | MAP Kinase Signaling System - genetics | TOR Serine-Threonine Kinases - genetics | Neoplasms - genetics | Aged, 80 and over | Adult | Female | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Adolescent | Aged | Mutation | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Science, ISSN 0036-8075, 3/2006, Volume 311, Issue 5765, pp. 1287 - 1290
Journal Article
Nature, ISSN 0028-0836, 05/2017, Volume 545, Issue 7653, pp. 175 - 180
Melanoma of the skin is a common cancer only in Europeans, whereas it arises in internal body surfaces (mucosal sites) and on the hands and feet (acral sites)... 
TERT PROMOTER MUTATIONS | UVEAL MELANOMA | SEQUENCE DATA | MULTIDISCIPLINARY SCIENCES | RECURRENT MUTATIONS | FREQUENT SOMATIC MUTATIONS | MALIGNANT-MELANOMA | GENERAL FRAMEWORK | CANCER GENOMES | ACTIVATING MUTATIONS | DRIVER MUTATIONS | Membrane Proteins - genetics | Humans | X-linked Nuclear Protein | Phosphoproteins - genetics | RNA Splicing Factors - genetics | Mutation - genetics | Genes, p16 | Genome, Human - genetics | Tumor Suppressor Protein p53 - genetics | Ultraviolet Rays - adverse effects | Telomerase - genetics | Signal Transduction - drug effects | GTP Phosphohydrolases - genetics | Melanoma - genetics | Proto-Oncogene Proteins B-raf - genetics | Mitogen-Activated Protein Kinases - genetics | Neurofibromatosis 1 - genetics | Melanoma - classification | Nuclear Proteins - genetics | DNA Helicases - genetics | Telomere - genetics | Genetic research | Genetic aspects | Genomes | Research | Melanoma | Pathogenesis | Copy number | Mucosa | p53 Protein | Radiation | Security | Epidemiology | Metastases | Reproduction (copying) | Coding | Mismatch repair | Clusters | Eye (anatomy) | Fellowships | Deoxyribonucleic acid--DNA | Medical research | Breakpoints | Radiation effects | MAP kinase | Exposure | Sun | Amplification | Bridges | Pathology | Ultraviolet radiation | Mutagenesis | Computation | Skin | Mutation | Internet | Aberration | Biotechnology | Genes | DNA damage | Carcinogens | Infrastructure | Signatures | Health | U.V. radiation | Inversions | Foldback | Data processing | Energy policy | Readers | Deamination | Protein kinase | Cell lines | Gene mapping | Tumors | Cancer | Index Medicus | Biological Science | 60 APPLIED LIFE SCIENCES
Journal Article
Nature, ISSN 0028-0836, 10/2008, Volume 455, Issue 7215, pp. 930 - 935
Journal Article