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Journal Article
PLoS ONE, ISSN 1932-6203, 01/2016, Volume 11, Issue 1, pp. e0146140 - e0146140
The common fruit fly Drosophila melanogaster (Dm) is a simple animal species that contributed significantly to the development of neurobiology whose... 
LOCALIZATION | PINK1 | GENE | MULTIDISCIPLINARY SCIENCES | MITOCHONDRIA | NEURONS | MUTATIONS | DYSFUNCTION | BRAIN | EARLY-ONSET PARKINSONISM | DEGENERATION | Single-Blind Method | Antiparkinson Agents - isolation & purification | Protein-Serine-Threonine Kinases - deficiency | Antiparkinson Agents - pharmacology | Plant Extracts - toxicity | Longevity - drug effects | Neuromuscular Junction - drug effects | Plant Extracts - pharmacology | Synaptic Potentials - drug effects | Antiparkinson Agents - toxicity | Mitochondria - ultrastructure | Antiparkinson Agents - therapeutic use | Parkinsonian Disorders - drug therapy | Reaction Time - drug effects | Endosomes - drug effects | Phytotherapy | Drug Evaluation, Preclinical | Ganglia, Invertebrate - ultrastructure | Locomotion - drug effects | Methanol | Parkinsonian Disorders - physiopathology | Ganglia, Invertebrate - drug effects | Protein-Serine-Threonine Kinases - genetics | Mitochondria - drug effects | Neuromuscular Junction - physiopathology | Drosophila melanogaster - drug effects | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Animals | Larva | Parkinsonian Disorders - pathology | Plant Roots - chemistry | Drosophila Proteins - deficiency | Drosophila melanogaster - growth & development | Drosophila Proteins - genetics | Plant Extracts - therapeutic use | Withania - chemistry | Care and treatment | Parkinson's disease | Drosophila | Dosage and administration | Research | Risk factors | Neurophysiology | Antiparkinsonian agents | Index Medicus
Journal Article
PLoS Computational Biology, ISSN 1553-734X, 09/2016, Volume 12, Issue 9, pp. e1005111 - e1005111
Journal Article
Nature, ISSN 0028-0836, 04/2015, Volume 520, Issue 7547, pp. 368 - 372
Drug resistance invariably limits the clinical efficacy of targeted therapy with kinase inhibitors against cancer(1,2). Here we show that targeted therapy with... 
CNS CELL-TYPES | MELANOMA | METASTASIS | MICROENVIRONMENT | TRANSLATIONAL PROFILING APPROACH | MULTIDISCIPLINARY SCIENCES | RAF INHIBITOR RESISTANCE | ACQUIRED-RESISTANCE | KINASE INHIBITORS | DRUG-RESISTANCE | CANCER CHEMORESISTANCE | Lung Neoplasms - drug therapy | Adenocarcinoma - pathology | Clone Cells - drug effects | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Proto-Oncogene Proteins c-fos - deficiency | Adenocarcinoma - metabolism | Neoplasm Metastasis - drug therapy | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Female | Proto-Oncogene Proteins c-akt - metabolism | Melanoma - metabolism | Tumor Microenvironment - drug effects | Cell Survival - drug effects | Melanoma - pathology | Down-Regulation - drug effects | Enzyme Activation - drug effects | Adenocarcinoma - drug therapy | Disease Progression | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Cell Movement - drug effects | Lung Neoplasms - secretion | Melanoma - secretion | Animals | Clone Cells - pathology | Metabolome - drug effects | Signal Transduction - drug effects | Neoplasm Metastasis - pathology | Protein Kinase Inhibitors - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Adenocarcinoma - secretion | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Pharmaceutical research | Care and treatment | Oncology, Experimental | Dosage and administration | Research | Drug therapy | Drug resistance | Antineoplastic agents | Tumors | Cancer | Melanoma | Mutation | Metastasis | Kinases | Cancer therapies | Index Medicus
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 | Receptor, Epidermal Growth Factor - genetics | Drug Resistance, Multiple - drug effects | Protein Conformation - drug effects | Lung Neoplasms - pathology | Receptor, Epidermal Growth Factor - metabolism | 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 | Lung Neoplasms - enzymology | Allosteric Site - drug effects | Mutant Proteins - genetics | Cetuximab - pharmacology | Mutant Proteins - metabolism | Receptor, Epidermal Growth Factor - chemistry | Drug Synergism | Drug Resistance, Neoplasm - genetics | Animals | Mutant Proteins - chemistry | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | 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 | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 06/2017, Volume 546, Issue 7658, pp. 431 - 435
Therapies that target signalling molecules that are mutated in cancers can often have substantial short-term effects, but the emergence of resistant cancer... 
METASTATIC MELANOMA | BRAF INHIBITOR | SUBPOPULATIONS | CHROMATIN | MULTIDISCIPLINARY SCIENCES | SINGLE MAMMALIAN-CELLS | STATE | MECHANISMS | MUTATIONS | VEMURAFENIB | PLASTICITY | Transcription, Genetic - drug effects | Humans | Male | Transcription Factor AP-1 - metabolism | DNA-Binding Proteins - metabolism | Melanoma - genetics | Female | Indoles - pharmacology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Single-Cell Analysis | Cellular Reprogramming - genetics | ErbB Receptors - metabolism | In Situ Hybridization, Fluorescence | Nuclear Proteins - metabolism | Signal Transduction - genetics | Melanoma - pathology | Sulfonamides - pharmacology | Cellular Reprogramming - drug effects | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Genetic Markers - drug effects | Vemurafenib | Drug Resistance, Neoplasm - genetics | Animals | Signal Transduction - drug effects | Genetic Markers - genetics | Cell Line, Tumor | Oncogene Protein p65(gag-jun) - metabolism | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Antimitotic agents | Cell interaction | Dosage and administration | Antineoplastic agents | Drug resistance | Observations | Health aspects | Subpopulations | Transcription factors | Substance abuse treatment | Variability | Activator protein 1 | Melanoma | Genomes | Kinases | Gene expression | Sox10 protein | Signal transduction | Signaling | Converting | Population | Mutation | Differentiation | Deoxyribonucleic acid--DNA | Cancer | Index Medicus
Journal Article
Blood, ISSN 0006-4971, 01/2006, Volume 107, Issue 2, pp. 752 - 759
Journal Article
Nature, ISSN 0028-0836, 01/2016, Volume 529, Issue 7584, pp. 110 - 114
Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas(1,2). Mutant IDH protein produces a new... 
MAINTENANCE | METHYLATION | LANDSCAPE | DEMETHYLATION | MULTIDISCIPLINARY SCIENCES | INTEGRATED GENOMIC ANALYSIS | ARCHITECTURE | PHENOTYPE | EXPRESSION | 2-HYDROXYGLUTARATE | PRINCIPLES | Chromatin - metabolism | Up-Regulation | Humans | Glioma - genetics | Base Sequence | Glioma - pathology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Chromatin - drug effects | Repressor Proteins - metabolism | Oncogenes - genetics | Insulator Elements - genetics | Glioma - enzymology | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Isocitrate Dehydrogenase - genetics | DNA Methylation - genetics | Down-Regulation - drug effects | Mutation - genetics | CRISPR-Cas Systems - genetics | Insulator Elements - drug effects | Phenotype | Isocitrate Dehydrogenase - chemistry | Receptor, Platelet-Derived Growth Factor alpha - genetics | CCCTC-Binding Factor | CpG Islands - genetics | Protein Binding | Isocitrate Dehydrogenase - metabolism | Cell Proliferation - drug effects | Enhancer Elements, Genetic - genetics | Glutarates - metabolism | Cell Transformation, Neoplastic - drug effects | Chromatin - genetics | DNA Methylation - drug effects | Glioma - drug therapy | Complications and side effects | Care and treatment | Platelet-derived growth factor | Gliomas | Analysis | Influence | Genetic aspects | Research | Methylation | Oncogenes | DNA methylation | Epigenetics | Genomes | Mutation | Gene expression | Binding sites | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article