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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 | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 2008, Volume 14, Issue 5, pp. 382 - 393
A key step in angiogenesis is the upregulation of growth factor receptors on endothelial cells. Here, we demonstrate that a small regulatory microRNA, miR-296,... 
CELLCYCLE | THERAPY | ONCOLOGY | VASCULAR INTEGRITY | IN-VIVO | GENE-EXPRESSION | DEGRADATION | TARGETS | OCULAR NEOVASCULARIZATION | TUMOR ANGIOGENESIS | MICRORNAS | CANCER | CELL BIOLOGY | Endothelium, Vascular - cytology | Luciferases - metabolism | MicroRNAs - antagonists & inhibitors | Humans | Neovascularization, Pathologic | Molecular Sequence Data | MicroRNAs - metabolism | Brain Neoplasms - blood supply | Phosphoproteins - antagonists & inhibitors | Phosphoproteins - metabolism | RNA, Messenger - metabolism | Receptor, Platelet-Derived Growth Factor beta - genetics | Brain Neoplasms - metabolism | Glioma - metabolism | Vascular Endothelial Growth Factor Receptor-2 - genetics | Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors | Kidney - metabolism | Receptor, Platelet-Derived Growth Factor beta - antagonists & inhibitors | Oligonucleotides - pharmacology | Base Sequence | RNA, Messenger - antagonists & inhibitors | Glioma - therapy | Umbilical Veins - cytology | Receptor, Platelet-Derived Growth Factor beta - metabolism | Signal Transduction | Endosomal Sorting Complexes Required for Transport | RNA, Messenger - genetics | RNA, Small Interfering - pharmacology | Cells, Cultured | Angiogenesis Inhibitors - pharmacology | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Kidney - cytology | Phosphoproteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Sequence Homology, Nucleic Acid | Blotting, Western | Hepatocyte Growth Factor - metabolism | Glioma - blood supply | Xenograft Model Antitumor Assays | Magnetic Resonance Imaging | Animals | Endothelium, Vascular - metabolism | Brain Neoplasms - therapy | Fluorescent Antibody Technique | Mice | MicroRNAs - genetics | Cell Movement | Umbilical Veins - metabolism | Tyrosine | Medical colleges | Neurosciences | Messenger RNA | Gliomas | Oncology, Experimental | Brain tumors | Research | Growth factors | Cancer | Endothelium | Index Medicus | PDGFR | VEGFR | miRNA | cancer | HGS | angiogenesis
Journal Article
Diabetes, ISSN 0012-1797, 05/2013, Volume 62, Issue 5, pp. 1453 - 1463
Glucagon, an essential regulator of glucose homeostasis, also modulates lipid metabolism and promotes weight loss, as reflected by the wasting observed in... 
PPAR-ALPHA | BODY-WEIGHT | METABOLISM | FIBROBLAST-GROWTH-FACTOR-21 | PHARMACOLOGY | INCREASES ENERGY-EXPENDITURE | ENDOCRINOLOGY & METABOLISM | DEGRADATION | MICE | INSULIN SENSITIVITY | FGF21 | Obesity - drug therapy | Humans | Peptides - pharmacokinetics | Fibroblast Growth Factors - genetics | Male | Fibroblast Growth Factors - secretion | Obesity - blood | Anti-Obesity Agents - therapeutic use | Glucagon - agonists | Fibroblast Growth Factors - metabolism | Anti-Obesity Agents - pharmacokinetics | Peptides - chemical synthesis | Hepatocytes - secretion | Hypoglycemic Agents - therapeutic use | Receptors, Glucagon - agonists | Receptors, Glucagon - genetics | Hypoglycemic Agents - pharmacokinetics | Peptides - physiology | Rats | Hypoglycemic Agents - pharmacology | Mice, Knockout | Cross-Over Studies | Anti-Obesity Agents - chemical synthesis | Mice | Anti-Obesity Agents - pharmacology | Hepatocytes - pathology | Diabetes Mellitus, Type 2 - metabolism | Hepatocytes - metabolism | Molecular Targeted Therapy | Mice, Mutant Strains | HEK293 Cells | Adult | Female | Hepatocytes - drug effects | Recombinant Proteins - metabolism | Double-Blind Method | Cells, Cultured | Insulin Resistance | Receptors, Glucagon - metabolism | Recombinant Proteins - agonists | Glucagon - pharmacology | Obesity - metabolism | Diabetes Mellitus, Type 2 - blood | Animals | Fibroblast Growth Factors - blood | Hypoglycemic Agents - chemical synthesis | Glucagon - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Peptides - therapeutic use | Physiological aspects | Fibroblast growth factors | Research | Glucagon | Analysis | Index Medicus | Abridged Index Medicus | Original Research
Journal Article
Hepatology, ISSN 0270-9139, 04/2014, Volume 59, Issue 4, pp. 1577 - 1590
Hepatocellular carcinoma (HCC) is the most rapidly increasing cause of cancer‐related mortality in the United States. Because of the lack of viable treatment... 
FUNCTIONAL POLYMORPHISM | HEPATIC STELLATE CELLS | MODELS | GENE-EXPRESSION | TARGETS | RISK | MECHANISMS | CYP2E1 | GASTROENTEROLOGY & HEPATOLOGY | ERLOTINIB | HEPATOCARCINOGENESIS | Erlotinib Hydrochloride | Prognosis | Rats, Wistar | Carcinoma, Hepatocellular - prevention & control | Humans | Transcriptome | Hepatic Stellate Cells - metabolism | Receptor, Epidermal Growth Factor - drug effects | Hepatocytes - pathology | Male | Receptor, Epidermal Growth Factor - metabolism | Diethylnitrosamine - adverse effects | Liver Neoplasms - pathology | Phosphorylation - drug effects | Liver Cirrhosis - genetics | Hepatic Stellate Cells - pathology | Hepatocytes - drug effects | Disease Models, Animal | Hepatic Stellate Cells - drug effects | Liver Neoplasms - prevention & control | Liver Cirrhosis - etiology | Liver Cirrhosis - prevention & control | Carbon Tetrachloride - adverse effects | Cells, Cultured | Bile Ducts - physiopathology | Rats | Mice, Inbred Strains | Disease Progression | Animals | Quinazolines - therapeutic use | Carcinoma, Hepatocellular - pathology | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Cell Proliferation - drug effects | Mice | Ligation - adverse effects | Quinazolines - pharmacology | Liver cancer | Epidermal growth factor | Rodents | Mortality | Hepatology | Gene expression | Liver cirrhosis | Index Medicus
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2012, Volume 109, Issue 8, pp. 3041 - 3046
Glioblastoma (GBM) is distinguished by a high degree of intratumoral heterogeneity, which extends to the pattern of expression and amplification of receptor... 
Tumor cell line | Glioma | Glioblastoma | Cell lines | Cell separation | Genetic mutation | Genotypes | Tumors | Cancer | Daughter cells | Mosaicism | Amplicon | Glioblastoma genetics | MULTIDISCIPLINARY SCIENCES | RECURRENT GLIOBLASTOMA | TUMORIGENICITY | CANCER | MULTIFORME | PHASE-II TRIAL | THERAPY | mosaicism | COPY NUMBER | glioma | GENE AMPLIFICATION | MALIGNANT GLIOMAS | amplicon | MEDULLOBLASTOMA | glioblastoma genetics | Receptor, Epidermal Growth Factor - genetics | Glioblastoma - enzymology | Cell Proliferation | Humans | In Situ Hybridization, Fluorescence | Genetic Heterogeneity | Genome, Human - genetics | Intercellular Signaling Peptides and Proteins - metabolism | Gene Amplification | Glioblastoma - genetics | Receptor, Platelet-Derived Growth Factor alpha - genetics | Computer Simulation | Glioblastoma - pathology | Chromosome Segregation - genetics | Tyrosine | Receptors | Blood platelets | Physiological aspects | Development and progression | Genetic aspects | Health aspects | Phosphotransferases | Glioblastoma multiforme | Molecules | Kinases | Cells | Deoxyribonucleic acid--DNA | Fluorescence in situ hybridization | Platelet-derived growth factor receptors | Epidermal growth factor receptors | Hepatocyte growth factor | Tumor cells | Clinical trials | Genomes | 1-Phosphatidylinositol 3-kinase | c-Met protein | Protein-tyrosine kinase receptors | Atlases | DNA sequencing | Index Medicus | Biological Sciences
Journal Article
Biomacromolecules, ISSN 1525-7797, 10/2012, Volume 13, Issue 10, pp. 3311 - 3319
Journal Article
Kidney International, ISSN 0085-2538, 11/2016, Volume 90, Issue 5, pp. 928 - 930
In chronic kidney disease, systemic inflammation is common and associated with mortality. The present study demonstrates that fibroblast growth factor 23... 
MORTALITY | UROLOGY & NEPHROLOGY | CHRONIC KIDNEY-DISEASE | CKD | LEFT-VENTRICULAR HYPERTROPHY | Renal Insufficiency, Chronic | Inflammation | Fibroblast Growth Factors | Hepatocytes | Humans | Index Medicus
Journal Article
Gastroenterology, ISSN 0016-5085, 2012, Volume 143, Issue 3, pp. 811 - 820.e15
Background & Aims Histone deacetylation regulates chromatin remodeling and transcriptional down-regulation of specific genomic regions; it is altered in many... 
Gastroenterology and Hepatology | Liver Cancer | RNA Processing | HGF | Mouse Model | HUMAN CANCER-CELLS | EPIGENETIC THERAPY | PATHWAY | C-MET | PROSTATE-CANCER | GENE-EXPRESSION | TARGETS | INHIBITORS | GASTROENTEROLOGY & HEPATOLOGY | UP-REGULATION | MIR-449A | Proto-Oncogene Proteins c-met - metabolism | Phosphorylation | Cell Proliferation | Humans | Gene Expression Regulation, Neoplastic | MicroRNAs - metabolism | Gene Expression Profiling | RNA, Messenger - metabolism | Transfection | RNA Interference | Time Factors | Carcinoma, Hepatocellular - genetics | HEK293 Cells | Liver Neoplasms - pathology | 3' Untranslated Regions | Liver Neoplasms - enzymology | Binding Sites | Hydroxamic Acids - pharmacology | Genes, Reporter | Histone Deacetylases - genetics | Liver Neoplasms - genetics | Histone Deacetylases - metabolism | Carcinoma, Hepatocellular - enzymology | Tumor Burden | Blotting, Western | Hep G2 Cells | Hepatocyte Growth Factor - metabolism | Proto-Oncogene Proteins c-met - genetics | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Mice, Nude | Carcinoma, Hepatocellular - pathology | Histone Deacetylase Inhibitors - pharmacology | Mice | Histone Deacetylase 2 - metabolism | Apoptosis | Histone Deacetylase 1 - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Liver cancer | Chromatin | MicroRNA | Messenger RNA | Analysis | Hepatoma | Genetic transcription | Tyrosine | Liver | Index Medicus | Abridged Index Medicus
Journal Article