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Nature reviews. Cancer, ISSN 1474-1768, 2017, Volume 17, Issue 2, pp. 93 - 115
Journal Article
The Journal of immunology (1950), ISSN 1550-6606, 2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors
Journal Article
Nature medicine, ISSN 1546-170X, 2013, Volume 19, Issue 4, pp. 446 - 451
Journal Article
The New England journal of medicine, ISSN 1533-4406, 2017, Volume 377, Issue 4, pp. 338 - 351
Journal Article
Nature reviews. Rheumatology, ISSN 1759-4804, 2017, Volume 13, Issue 4, pp. 217 - 233
TNF blockers are highly efficacious at dampening inflammation and reducing symptoms in rheumatic diseases such as rheumatoid arthritis, psoriatic arthritis and... 
LIGAND 1A TL1A | COLLAGEN-INDUCED ARTHRITIS | FIBROBLAST-LIKE SYNOVIOCYTES | TUMOR-NECROSIS-FACTOR | SYSTEMIC-LUPUS-ERYTHEMATOSUS | LYMPHOTOXIN-BETA-RECEPTOR | SYNOVIAL FIBROBLASTS | CD4(+) T-CELLS | CD40 LIGAND | MONOCLONAL-ANTIBODY | RHEUMATOLOGY | Fas Ligand Protein - metabolism | Rheumatic Diseases - drug therapy | OX40 Ligand - metabolism | CD27 Ligand - antagonists & inhibitors | Dendritic Cells - immunology | Humans | Lymphotoxin-alpha - metabolism | Molecular Targeted Therapy | 4-1BB Ligand - antagonists & inhibitors | TNF-Related Apoptosis-Inducing Ligand - antagonists & inhibitors | CD40 Ligand - metabolism | CD27 Ligand - metabolism | Cell Death | Rheumatic Diseases - immunology | Signal Transduction | Lymphocyte Activation | Tumor Necrosis Factors - metabolism | 4-1BB Ligand - metabolism | Immune Tolerance | Tumor Necrosis Factor Ligand Superfamily Member 15 - metabolism | TNF-Related Apoptosis-Inducing Ligand - metabolism | Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism | Tumor Necrosis Factors - immunology | OX40 Ligand - antagonists & inhibitors | Cytokine TWEAK | Fas Ligand Protein - antagonists & inhibitors | Animals | Tumor Necrosis Factor Ligand Superfamily Member 15 - antagonists & inhibitors | T-Lymphocytes - immunology | Tumor Necrosis Factor Ligand Superfamily Member 14 - antagonists & inhibitors | CD40 Ligand - antagonists & inhibitors | Lymphotoxin-alpha - antagonists & inhibitors | Tumor Necrosis Factors - antagonists & inhibitors | Care and treatment | Cytokines | Tumor necrosis factor | Rheumatic diseases | Development and progression | Genetic aspects | Health aspects
Journal Article
Cancer discovery, ISSN 2159-8290, 2017, Volume 7, Issue 4, pp. 400 - 409
Entrectinib, a potent oral inhibitor of the tyrosine kinases TRKA/B/C, ROS1, and ALK, was evaluated in two phase I studies in patients with advanced or... 
REARRANGEMENT | ONCOGENE | ONCOLOGY | ANALOG SECRETORY CARCINOMA | LANDSCAPE | KINASE FUSIONS | SARCOMAS | ETV6-NTRK3 GENE FUSION | CRIZOTINIB | GENOMIC ALTERATIONS | CLINICAL-RESPONSE | Benzamides - pharmacokinetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Receptor, trkA - antagonists & inhibitors | Male | Receptor, trkB - genetics | Indazoles - administration & dosage | Protein Kinase Inhibitors - adverse effects | Mammary Analogue Secretory Carcinoma - genetics | Dose-Response Relationship, Drug | Benzamides - administration & dosage | Membrane Glycoproteins - antagonists & inhibitors | Receptor, trkC - genetics | Anaplastic Lymphoma Kinase | Melanoma - genetics | Colorectal Neoplasms - drug therapy | Receptor, trkB - antagonists & inhibitors | Aged, 80 and over | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Benzamides - adverse effects | Carcinoma, Non-Small-Cell Lung - pathology | Crizotinib | Protein Kinase Inhibitors - pharmacokinetics | Proto-Oncogene Proteins - antagonists & inhibitors | Pyridines - administration & dosage | Carcinoma, Non-Small-Cell Lung - genetics | Receptor, trkC - antagonists & inhibitors | Melanoma - pathology | Mammary Analogue Secretory Carcinoma - drug therapy | Membrane Glycoproteins - genetics | Protein Kinase Inhibitors - administration & dosage | Sequestosome-1 Protein - genetics | Pyrazoles - administration & dosage | Indazoles - pharmacokinetics | Receptor Protein-Tyrosine Kinases - genetics | Oncogene Proteins, Fusion - genetics | Melanoma - drug therapy | Adolescent | Receptor, trkA - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Indazoles - adverse effects | Colorectal Neoplasms - pathology | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Leukemia, ISSN 1476-5551, 2008, Volume 23, Issue 3, pp. 477 - 485
The detailed molecular mechanism of action of second-generation BCR-ABL tyrosine kinase inhibitors, including perturbed targets and pathways, should contribute... 
BCR-ABL INHIBITORS | SRC | TYROSINE KINASE | MECHANISMS | NILOTINIB | BREAST-CANCER CELLS | dasatinib | ONCOLOGY | IMATINIB | kinase profiling | RESISTANCE | chronic myeloid leukemia | chemical proteomics | SKI-606 | HEMATOLOGY | bosutinib | Nitriles - pharmacology | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Substrate Specificity | Neoplasm Proteins - antagonists & inhibitors | Gene Expression Profiling | K562 Cells - drug effects | Quinolines - pharmacology | Drug Delivery Systems | Leukemia, Myeloid, Accelerated Phase - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Dasatinib | Nerve Tissue Proteins - antagonists & inhibitors | Aniline Compounds - pharmacology | Leukocytes, Mononuclear - drug effects | Quinolines - chemistry | src-Family Kinases - antagonists & inhibitors | Pyrimidines - pharmacology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors | K562 Cells - enzymology | Leukemia, Myeloid, Accelerated Phase - enzymology | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Fusion Proteins, bcr-abl - antagonists & inhibitors | Nitriles - chemistry | Leukocytes, Mononuclear - enzymology | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Aniline Compounds - chemistry | Drug Screening Assays, Antitumor | Protein-Tyrosine Kinases - antagonists & inhibitors | Enzyme inhibitors | Physiological aspects | Chronic myeloid leukemia | Research | Drug therapy | Health aspects | Protein kinases
Journal Article