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Nature (London), ISSN 1476-4687, 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... 
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 | Anaplastic Lymphoma Kinase | 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 | ErbB Receptors - antagonists & inhibitors | 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 | 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 | 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
Journal Article
Nature neuroscience, ISSN 1546-1726, 2013, Volume 16, Issue 2, pp. 183 - 192
A major unresolved issue in treating pain is the paradoxical hyperalgesia produced by the gold-standard analgesic morphine and other opiates. We found that... 
LAMINA-I NEURONS | NEUROTROPHIC FACTOR | P2X RECEPTORS | DOWN-REGULATION | OPIOID-RECEPTOR GENE | SPINAL-CORD-INJURY | UNDERLYING NEUROPATHIC PAIN | ALTERED CHLORIDE HOMEOSTASIS | NERVE INJURY | NEUROSCIENCES | INDUCED ABNORMAL PAIN | Brain-Derived Neurotrophic Factor - genetics | Biophysical Phenomena - drug effects | Motor Activity - drug effects | Male | Ribosome Inactivating Proteins, Type 1 - pharmacology | Touch | CD11b Antigen - genetics | Microglia - physiology | Time Factors | Chlorides - metabolism | Pain Threshold - drug effects | Biophysical Phenomena - genetics | Vocalization, Animal - drug effects | Brain-Derived Neurotrophic Factor - metabolism | Homeostasis - drug effects | Protein Synthesis Inhibitors - pharmacology | Spinal Cord - cytology | Neurons - drug effects | Membrane Potentials - drug effects | Hot Temperature - adverse effects | Microglia - drug effects | Mice, Inbred C57BL | Rats | Mice, Transgenic | Signal Transduction - genetics | Down-Regulation - drug effects | Rats, Sprague-Dawley | Symporters - metabolism | Gene Expression Regulation - drug effects | Narcotics - administration & dosage | Patch-Clamp Techniques | Rotarod Performance Test | Animals | Hyperalgesia - drug therapy | Signal Transduction - drug effects | Naloxone - pharmacology | Narcotic Antagonists - pharmacology | Mice | CD11b Antigen - metabolism | Receptors, Purinergic P2X4 - metabolism | Morphine - administration & dosage | Receptors, Purinergic P2X4 - genetics | Ion Channel Gating - drug effects
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2015, Volume 10, Issue 1, p. e0116747
Cellular mechanisms of multidrug resistance (MDR) are related to ABC transporters, apoptosis, antioxidation, drug metabolism, DNA repair and cell proliferation... 
EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER CELLS | STEM-CELLS | MDR1 | TRANSPORTERS | MULTIDISCIPLINARY SCIENCES | DOWN-REGULATION | MUTANT P53 | TUMOR-SUPPRESSOR PROTEIN | DRUG-RESISTANCE | OVARIAN-CANCER | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Drug Resistance, Multiple - drug effects | Genes, Neoplasm | Humans | Apoptosis - genetics | Epithelial-Mesenchymal Transition - drug effects | Gene Expression Profiling | DNA Repair - genetics | Epithelial-Mesenchymal Transition - genetics | Neoplasm Proteins - metabolism | Dose-Response Relationship, Drug | MCF-7 Cells | Neoplastic Stem Cells - metabolism | Inhibitory Concentration 50 | Gene Expression Regulation, Neoplastic - drug effects | Neoplasm Proteins - genetics | DNA Repair - drug effects | Drug Resistance, Multiple - genetics | Tumor Suppressor Protein p53 - metabolism | Signal Transduction - genetics | Down-Regulation - drug effects | Cell Shape - drug effects | Up-Regulation - drug effects | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - genetics | Signal Transduction - drug effects | Doxorubicin - pharmacology | Drug Resistance, Neoplasm - drug effects | Physiological aspects | Drug resistance in microorganisms | Anthracyclines | Tumor proteins | Intermediate filament proteins | Genes | Cell proliferation | Transcription | Bcl-2 protein | Mesenchyme | Gene regulation | Cytology | AKT protein | Cytotoxicity | Drug resistance | Kinases | DNA repair | Cancer therapies | Doxorubicin | Cell surface | E-cadherin | Cell morphology | Proteins | MDR1 protein | Clonal deletion | CD44 antigen | Rodents | Cell cycle | Drug metabolism | Repair | Drug dosages | Pharmaceutical sciences | Deoxyribonucleic acid--DNA | Glutathione | Enzymes | Ploidy | BRCA1 protein | Multidrug resistance | Breast cancer | Gene expression | Metabolism | 1-Phosphatidylinositol 3-kinase | Medicine | Hypotheses | Chemotherapy | Gene amplification | Pharmacy | Stem cells | Mutation | Codons | Surface markers | Apoptosis | Tumors | Deoxyribonucleic acid | DNA
Journal Article
Gastroenterology, ISSN 0016-5085, 2014, Volume 146, Issue 7, pp. 1763 - 1774
Background & Aims The NACHT, LRR, and pyrin domain–containing protein 3 (NLRP3) inflammasome induces inflammation in response to organ injury, but little is... 
Gastroenterology and Hepatology | Innate Immune Response | Immune Regulation | Pancreas | Mouse Model | ACTIVATION | NLRP3 INFLAMMASOME | GPR81 | AGONISTS | GENE | TLR9 | MICE | HEPATOTOXICITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | SEVERITY | Liver - pathology | Inflammasomes - metabolism | Receptors, G-Protein-Coupled - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Male | NF-kappa B - metabolism | Monocytes - immunology | Lipopolysaccharides | Liver - immunology | Liver - drug effects | RNA Interference | Interleukin-1beta - metabolism | Toll-Like Receptors - drug effects | Anti-Inflammatory Agents - administration & dosage | Toll-Like Receptors - metabolism | Cytoprotection | Disease Models, Animal | Galactosamine | Chemical and Drug Induced Liver Injury - prevention & control | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Liver - metabolism | Injections, Intraperitoneal | Pancreas - pathology | Pancreas - metabolism | Pancreas - immunology | Toll-Like Receptor 4 - metabolism | Chemical and Drug Induced Liver Injury - immunology | Monocytes - drug effects | Macrophages - metabolism | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Sodium Lactate - pharmacology | beta-Arrestins | Mice | Receptors, G-Protein-Coupled - genetics | RNA, Small Interfering - metabolism | Monocytes - metabolism | Pancreatitis - prevention & control | Arrestins - metabolism | Dose-Response Relationship, Drug | Pancreatitis - genetics | Transfection | Inflammasomes - drug effects | Sodium Lactate - administration & dosage | Pancreatitis - immunology | Chemical and Drug Induced Liver Injury - pathology | Chemical and Drug Induced Liver Injury - etiology | Macrophages - immunology | Cell Line | Immunity, Innate - drug effects | Toll-Like Receptor 4 - drug effects | Mice, Inbred C57BL | Pancreas - drug effects | Chemical and Drug Induced Liver Injury - genetics | Pancreatitis - chemically induced | Animals | Carrier Proteins - metabolism | beta-Arrestin 2 | Inflammasomes - immunology | Macrophages - drug effects | Pancreatitis - pathology | Pancreatitis - metabolism | Ceruletide | Lactates | Gastrointestinal diseases | Inflammation
Journal Article
Autophagy, ISSN 1554-8627, 05/2012, Volume 8, Issue 5, pp. 812 - 825
.... Furthermore, our results revealed that curcumin causes some novel cellular mechanisms that promote autophagy as a protective effect... 
autophagy | endothelial cell | FOXO1 | oxidative stress | curcumin | Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Oxidative stress | Endothelial cell | Curcumin | Autophagy | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | Phosphatidylinositol 3-Kinases - metabolism | Protein Transport - drug effects | Autophagy - drug effects | Gene Knockdown Techniques | Proto-Oncogene Proteins c-bcl-2 - metabolism | Cell Nucleus - metabolism | Forkhead Transcription Factors - metabolism | Protective Agents - pharmacology | Protein Binding - drug effects | Cytoprotection - drug effects | Membrane Proteins - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Beclin-1 | Hydrogen Peroxide - toxicity | rab GTP-Binding Proteins - metabolism | Cell Survival - drug effects | Human Umbilical Vein Endothelial Cells - drug effects | Curcumin - pharmacology | Down-Regulation - drug effects | Ubiquitin-Activating Enzymes - metabolism | Apoptosis Regulatory Proteins - metabolism | Up-Regulation - drug effects | Acetylation - drug effects | Autophagy-Related Protein 7 | Human Umbilical Vein Endothelial Cells - enzymology | Signal Transduction - drug effects | Models, Biological | Human Umbilical Vein Endothelial Cells - pathology | Forkhead Box Protein O1 | Oxidative Stress - drug effects | Cell Nucleus - drug effects | CELL BIOLOGY
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 08/2015, Volume 112, Issue 32, pp. 10038 - 10043
Colorectal cancer risk is associated with diets high in red meat. Heme, the pigment of red meat, induces cytotoxicity of colonic contents and elicits... 
Immunohistochemistry | Up-Regulation | Body Weight | Cell Proliferation | Biological Markers | Male | Mucus | Colony Count, Microbial | Journal Article | Antioxidants | Sulfides | Anti-Bacterial Agents | Microbiota | Ki-67 Antigen | Cell Death | Heme | Colon | Feces | Intestinal Mucosa | Down-Regulation | Mice, Inbred C57BL | Epithelial Cells | Animals | Cell Cycle | Diet | Models, Biological | Research Support, Non-U.S. Gov't | Mucolysis | (Tri)sulfides | Red meat | Mucus barrier | Colorectal cancer | colorectal cancer | MUCIN | MULTIDISCIPLINARY SCIENCES | SUSCEPTIBILITY | red meat | mucus barrier | (tri)sulfides | mucolysis | COLORECTAL-CANCER | CALCIUM | FAT | MICE | INHIBITOR | CYTOTOXICITY | EXPRESSION | Cell Cycle - genetics | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Colon - drug effects | Microbiota - drug effects | Body Weight - drug effects | Ki-67 Antigen - metabolism | Mucus - drug effects | Intestinal Mucosa - drug effects | Feces - microbiology | Heme - pharmacology | Mucus - metabolism | Sulfides - metabolism | Cell Death - drug effects | Biomarkers - metabolism | Colon - pathology | Epithelial Cells - pathology | Up-Regulation - genetics | Antioxidants - pharmacology | Intestinal Mucosa - microbiology | Down-Regulation - drug effects | Down-Regulation - genetics | Up-Regulation - drug effects | Anti-Bacterial Agents - pharmacology | Cell Proliferation - drug effects | Colon - microbiology | Cell Cycle - drug effects | Intestinal Mucosa - pathology | Cell proliferation | Colon cancer | Epithelial cells | Physiological aspects | Observations | Health aspects | Biological Sciences | susceptibility | expression | bacterial | inhibitor | mucin | fat | colorectal-cancer | mice | cytotoxicity
Journal Article
British journal of cancer, ISSN 1532-1827, 2009, Volume 100, Issue 9, pp. 1425 - 1433
Curcumin has been shown to inhibit the growth of various types of cancer cells; however, at concentrations much above the clinically achievable levels in... 
Curcumin | Chk1 | G2/M arrest | DNA damage | Pancreatic cancer | CARCINOMA-CELLS | DNA-DAMAGE | DOWN-REGULATION | REGULATED GENE-PRODUCTS | FACTOR-KAPPA-B | BENZYL ISOTHIOCYANATE | I CLINICAL-TRIAL | pancreatic cancer | ONCOLOGY | PROSTATE-CANCER | CHEMOPREVENTIVE AGENT | curcumin | Cell Cycle Proteins - drug effects | Protein Kinases - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Protein Kinases - genetics | Gene Silencing - drug effects | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Collagen Type XI - metabolism | DNA-Binding Proteins - metabolism | Pancreatic Neoplasms - drug therapy | Transfection | Tumor Suppressor Proteins - genetics | Caspase 3 - drug effects | Cell Cycle Proteins - genetics | Gene Expression Regulation, Neoplastic - drug effects | Protein-Serine-Threonine Kinases - metabolism | DNA Damage - drug effects | Protein Kinases - drug effects | Tumor Suppressor Proteins - metabolism | Collagen Type XI - drug effects | Pancreatic Neoplasms - pathology | Cell Cycle Proteins - metabolism | Curcumin - pharmacology | DNA-Binding Proteins - drug effects | Pancreatic Neoplasms - enzymology | Protein-Serine-Threonine Kinases - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Cell Division - drug effects | Protein-Serine-Threonine Kinases - drug effects | Cell Line, Tumor | Checkpoint Kinase 1 | Tumor Suppressor Proteins - drug effects | Cell Cycle - drug effects | Translational Therapeutics | M arrest
Journal Article
CELL DEATH & DISEASE, ISSN 2041-4889, 01/2018, Volume 9, Issue 2, pp. 96 - 15
Journal Article
Cell stem cell, ISSN 1934-5909, 2017, Volume 20, Issue 1, pp. 56 - 69
Satellite cells, the predominant stem cell population in adult skeletal muscle, are activated in response to hypertrophic stimuli and give rise to myogenic... 
hypertrophy | Pax7 | exosomes | muscle | collagen | microRNA | fibrosis | muscle progenitor cells | extracellular matrix | satellite cells | FIBROSIS | REGENERATION | GENE-EXPRESSION | EXOSOMES | SELF-RENEWAL | DUCHENNE MUSCULAR-DYSTROPHY | MIRNAS | SATELLITE CELL | DIFFERENTIATION | CONNECTIVE-TISSUE | CELL & TISSUE ENGINEERING | CELL BIOLOGY | Exosomes - drug effects | Exosomes - metabolism | NIH 3T3 Cells | Cell Survival - genetics | Extracellular Matrix - metabolism | MicroRNAs - metabolism | PAX7 Transcription Factor - metabolism | Muscle Fibers, Skeletal - drug effects | Muscle Fibers, Skeletal - metabolism | Stem Cells - metabolism | Gene Knockdown Techniques | Cell Differentiation - genetics | Extracellular Matrix - genetics | Cell Nucleus - metabolism | Gene Deletion | Collagen - genetics | Fibroblasts - metabolism | Cell Survival - drug effects | Ribonuclease III - metabolism | Extracellular Matrix - drug effects | Satellite Cells, Skeletal Muscle - metabolism | Down-Regulation - drug effects | Fibroblasts - pathology | Down-Regulation - genetics | Collagen - metabolism | Satellite Cells, Skeletal Muscle - drug effects | Animals | Carrier Proteins - metabolism | Muscle Development - drug effects | Cell Differentiation - drug effects | Models, Biological | Fibroblasts - drug effects | Muscle Fibers, Skeletal - pathology | Tamoxifen - pharmacology | Muscle Development - genetics | Stem Cells - drug effects | Mice | MicroRNAs - genetics | Muscle, Skeletal - pathology | Cell Nucleus - drug effects | Hypertrophy | miRNA | Dicer | Muscle extracellular matrix
Journal Article
Nature (London), ISSN 1476-4687, 2015, 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
Journal Article