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Cancer Cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, deletion and activation of results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and... 
CELLCYCLE | SIGNALING | EPITHELIAL-MESENCHYMAL TRANSITION | ONCOGENIC K-RAS | CANCER-CELLS | SUPPRESSOR | GENE | ONCOLOGY | SRC | KINASE INHIBITOR | EXPRESSION PROFILES | MUTATIONS | TUMORIGENESIS | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 08/2012, Volume 22, Issue 2, pp. 153 - 166
Genomic profiling has identified a subtype of high-risk B-progenitor acute lymphoblastic leukemia (B-ALL) with alteration of , a gene expression profile... 
GROWTH-FACTOR RECEPTOR | BCR-JAK2 FUSION GENE | ONCOLOGY | NUCLEAR-PORE | MYELOPROLIFERATIVE NEOPLASMS | ACUTE MYELOID-LEUKEMIA | OF-FUNCTION MUTATIONS | FLT3 MUTATIONS | CHILDHOOD | B-PROGENITOR | CHRONIC MYELOMONOCYTIC LEUKEMIA | CELL BIOLOGY | Recurrence | Humans | Molecular Sequence Data | RNA, Messenger - metabolism | Receptor, Platelet-Derived Growth Factor beta - genetics | Protein-Tyrosine Kinases - genetics | DNA Mutational Analysis | Base Sequence | Trans-Activators - genetics | Phosphorylation - drug effects | Philadelphia Chromosome | Receptors, Cytokine - genetics | Genetic Predisposition to Disease | RNA, Messenger - genetics | Risk Factors | Gene Expression Regulation, Leukemic - drug effects | Signal Transduction - genetics | Enzyme Activation - drug effects | Mutation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Animals | Signal Transduction - drug effects | Cell Transformation, Neoplastic | Oncogene Proteins, Fusion - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - enzymology | Mice | Protein Kinase Inhibitors - pharmacology | Gene Rearrangement - genetics | Sequence Deletion - genetics | Tyrosine | Platelet-derived growth factor | Cytokines | Genes | Oncology, Experimental | Genomes | Research | Gene expression | Population genetics | Hunger | Medical genetics | Genetic research | Nucleotide sequencing | Acute lymphocytic leukemia | Cancer | DNA sequencing | Index Medicus
Journal Article
Nature Immunology, ISSN 1529-2908, 03/2015, Volume 16, Issue 4, pp. 354 - 365
Interleukin 37 (IL-37) and IL-1R8 (SIGIRR or TIR8) are anti-inflammatory orphan members of the IL-1 ligand family and IL-1 receptor family, respectively. Here... 
CELLS | FAMILY-MEMBER | INFLAMMATION | TIR8/SIGIRR | INFECTION | IMMUNOLOGY | TOLL | INHIBITOR | EXPRESSION | NEGATIVE REGULATOR | MOLECULES | Inflammation - pathology | Interleukin-1 - genetics | RNA, Small Interfering - genetics | RNA-Binding Proteins - genetics | Humans | Receptors, Interleukin-1 - genetics | NF-kappa B - immunology | Receptor Protein-Tyrosine Kinases - immunology | Proto-Oncogene Proteins c-fyn - genetics | Signal Transduction - immunology | TOR Serine-Threonine Kinases - genetics | PTEN Phosphohydrolase - immunology | RNA, Small Interfering - immunology | Receptors, Interleukin-1 - deficiency | Leukocytes, Mononuclear - immunology | c-Mer Tyrosine Kinase | Interleukin-1 - immunology | Interleukin-18 Receptor alpha Subunit - genetics | Proto-Oncogene Proteins - immunology | Proto-Oncogene Proteins c-fyn - immunology | STAT3 Transcription Factor - genetics | Cell Line | PTEN Phosphohydrolase - genetics | Interleukin-18 Receptor alpha Subunit - immunology | Leukocytes, Mononuclear - drug effects | MAP Kinase Kinase Kinases - genetics | Receptors, Interleukin-1 - immunology | RNA-Binding Proteins - immunology | Gene Expression Regulation | Mice, Transgenic | Proto-Oncogene Proteins - genetics | Inflammation - immunology | Immunity, Innate | MAP Kinase Kinase Kinases - immunology | Interleukin-18 Receptor alpha Subunit - antagonists & inhibitors | Leukocytes, Mononuclear - pathology | TOR Serine-Threonine Kinases - immunology | Animals | NF-kappa B - genetics | Receptor Protein-Tyrosine Kinases - genetics | Lipopolysaccharides - pharmacology | Inflammation - genetics | Protein Binding | Mice | STAT3 Transcription Factor - immunology | Receptors, Interleukin-1 - antagonists & inhibitors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2013, Volume 502, Issue 7471, pp. 333 - 339
Journal Article
Blood, ISSN 0006-4971, 06/2011, Volume 117, Issue 23, pp. 6287 - 6296
B-cell receptor (BCR) signaling is aberrantly activated in chronic lymphocytic leukemia (CLL). Bruton tyrosine kinase (BTK) is essential to BCR signaling and... 
B-CELLS | CLL | FLUDARABINE PLUS CYCLOPHOSPHAMIDE | APOPTOTIC CELL-DEATH | RITUXIMAB | SURVIVAL SIGNALS | LYMPHOMA | DRUG-RESISTANCE | INHIBITOR | HEMATOLOGY | EXPRESSION | T-Lymphocytes - enzymology | Apoptosis - drug effects | Humans | Tumor Necrosis Factor-alpha - genetics | Cell Survival - genetics | Apoptosis - genetics | Male | NF-kappa B - metabolism | Neoplasm Proteins - antagonists & inhibitors | Receptors, Antigen, B-Cell - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Neoplasm Proteins - genetics | Interleukin-6 - metabolism | Cell Survival - drug effects | Drug Screening Assays, Antitumor - methods | Interleukin-6 - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Gene Expression Regulation, Leukemic - drug effects | Pyrimidines - pharmacology | Leukemia, Lymphocytic, Chronic, B-Cell - enzymology | B-Cell Activating Factor - metabolism | CD40 Ligand - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Gene Expression Regulation, Enzymologic - genetics | Cell Line, Tumor | Receptors, Antigen, B-Cell - genetics | Mice | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Mitogen-Activated Protein Kinase 1 - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Gene Expression Regulation, Leukemic - genetics | Protein-Tyrosine Kinases - genetics | CD40 Ligand - metabolism | MAP Kinase Signaling System - genetics | Female | Interleukin-4 - genetics | Protein-Tyrosine Kinases - biosynthesis | Pyrazoles - pharmacology | B-Lymphocytes - enzymology | Neoplasm Proteins - biosynthesis | Interleukin-4 - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | MAP Kinase Signaling System - drug effects | NF-kappa B - genetics | B-Cell Activating Factor - genetics | Cell Proliferation - drug effects | Index Medicus | Abridged Index Medicus | Lymphoid Neoplasia
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 10/2010, Volume 363, Issue 18, pp. 1693 - 1703
A small group of patients with non–small-cell lung cancer have genetic lesions that activate anaplastic lymphoma kinase (ALK). Crizotinib, an orally... 
ALK | MEDICINE, GENERAL & INTERNAL | GEFITINIB | EML4-ALK FUSION GENE | 2ND-LINE TREATMENT | PHASE-II | EGFR MUTATIONS | IDENTIFICATION | TUMORS | ACTIVATING MUTATIONS | IMMUNOHISTOCHEMISTRY | Lung Neoplasms - drug therapy | Pyrazoles - therapeutic use | Microtubule-Associated Proteins - genetics | Humans | Middle Aged | Receptors, Growth Factor - antagonists & inhibitors | Lung Neoplasms - pathology | Male | Protein Kinase Inhibitors - adverse effects | Protein-Tyrosine Kinases - genetics | Pyridines - adverse effects | Serine Endopeptidases - genetics | Cell Cycle Proteins - genetics | Adult | Female | Pyrazoles - adverse effects | Pyridines - therapeutic use | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Pyridines - administration & dosage | Administration, Oral | Carcinoma, Non-Small-Cell Lung - genetics | Proto-Oncogene Proteins c-met - antagonists & inhibitors | Kaplan-Meier Estimate | In Situ Hybridization, Fluorescence | Receptor Protein-Tyrosine Kinases | Disease Progression | Protein Kinase Inhibitors - administration & dosage | Pyrazoles - administration & dosage | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Protein-Tyrosine Kinases - antagonists & inhibitors | Tyrosine | Care and treatment | Lung cancer, Small cell | Genetic aspects | Diagnosis | Health aspects | Phosphotransferases | Lymphomas | Pharmaceutical industry | Lung cancer | Tumors | Index Medicus | Abridged Index Medicus
Journal Article
Nature Genetics, ISSN 1061-4036, 08/2012, Volume 44, Issue 8, pp. 852 - 860
Human non-small cell lung cancers (NSCLCs) with activating mutations in EGFR frequently respond to treatment with EGFRtargeted tyrosine kinase inhibitors... 
GEFITINIB | RECEPTOR TYROSINE KINASES | MET AMPLIFICATION | GROWTH | GENETICS & HEREDITY | ACQUIRED-RESISTANCE | MUTATIONS | NF-KAPPA-B | TUMORS | MUTANT EGFR | ERLOTINIB | Erlotinib Hydrochloride | Proto-Oncogene Proteins c-met - metabolism | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Humans | Lung Neoplasms - metabolism | Middle Aged | Lung Neoplasms - pathology | Male | Intercellular Signaling Peptides and Proteins - metabolism | Epithelial-Mesenchymal Transition | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Proto-Oncogene Proteins - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins c-met - genetics | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Receptor Protein-Tyrosine Kinases - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Enzyme Activation | Mutation | Quinazolines - pharmacology | Erlotinib | Physiological aspects | Genetic aspects | Research | Lung cancer, Non-small cell | Drug therapy | Health aspects | Protein kinases | Studies | Medical research | Rodents | Lung cancer | Genomics | Kinases | Gene expression | Acquisitions & mergers | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 08/2007, Volume 448, Issue 7153, pp. 561 - 566
Improvement in the clinical outcome of lung cancer is likely to be achieved by identification of the molecular events that underlie its pathogenesis. Here we... 
ANAPLASTIC LYMPHOMA KINASE | FACTOR-RECEPTOR | ALK | GEFITINIB | TRANSLOCATIONS | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | COMMON | PROLIFERATION | MUTATIONS | INHIBITOR | Lung Neoplasms - drug therapy | Oncogene Proteins, Fusion - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Lung Neoplasms - metabolism | Molecular Sequence Data | Lung Neoplasms - pathology | Chromosomes, Human, Pair 2 - genetics | Protein-Tyrosine Kinases - genetics | Oncogene Proteins, Fusion - chemistry | Cell Transformation, Neoplastic - genetics | Serine Endopeptidases - genetics | Cell Cycle Proteins - genetics | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Amino Acid Sequence | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Cell Cycle Proteins - metabolism | Mutation - genetics | Receptor Protein-Tyrosine Kinases | Animals | Oncogene Proteins, Fusion - genetics | Oncogene Proteins, Fusion - antagonists & inhibitors | Cell Proliferation - drug effects | Mice | Serine Endopeptidases - metabolism | Carcinoma, Non-Small-Cell Lung - drug therapy | Cell Transformation, Neoplastic - pathology | 3T3 Cells | Chromosome Inversion - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | Genetics | Molecular biology | Kinases | Lung cancer | Rodents | Index Medicus
Journal Article