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Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
Journal Article
The American Journal of Human Genetics, ISSN 0002-9297, 2007, Volume 80, Issue 3, pp. 550 - 560
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, ISSN 0028-0836, 08/2011, Volume 476, Issue 7360, pp. 298 - 303
Journal Article
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
Neuron, ISSN 0896-6273, 04/2013, Volume 78, Issue 1, pp. 57 - 64
Valosin-containing protein (VCP) is a highly expressed member of the type II AAA+ ATPase family. mutations are the cause of inclusion body myopathy, Paget’s... 
LIPID-PEROXIDATION | SPINAL-CORD PATHOLOGY | MOUSE MODEL | ALS | AMYOTROPHIC-LATERAL-SCLEROSIS | DYSFUNCTION | BONE | NEUROSCIENCES | PAGET-DISEASE | TRANSGENIC MICE | REVEALS | RNA, Small Interfering - genetics | Humans | Middle Aged | Male | Frontotemporal Dementia - metabolism | Neurons - ultrastructure | Muscular Dystrophies, Limb-Girdle - genetics | Adenosine Triphosphate - metabolism | Membrane Potential, Mitochondrial - genetics | Muscular Dystrophies, Limb-Girdle - pathology | NAD - metabolism | Fibroblasts - metabolism | Animals, Newborn | Frontotemporal Dementia - genetics | Magnesium - metabolism | Mitochondria - pathology | Fibroblasts - pathology | Mutation - genetics | Myositis, Inclusion Body - genetics | Osteitis Deformans - pathology | Muscular Dystrophies, Limb-Girdle - metabolism | Analysis of Variance | Luminescent Proteins - genetics | Adenosine Triphosphatases - genetics | Mice | Lipid Peroxidation - genetics | RNA, Small Interfering - metabolism | Valosin Containing Protein | Osteitis Deformans - metabolism | Family Health | Cerebral Cortex - cytology | Case-Control Studies | Osteitis Deformans - genetics | Transfection | Mitochondria - genetics | Cell Cycle Proteins - genetics | Myositis, Inclusion Body - pathology | Adult | Female | Neuroblastoma - pathology | Frontotemporal Dementia - pathology | Adenosine Triphosphatases - deficiency | Mice, Inbred C57BL | Cells, Cultured | Cell Cycle Proteins - deficiency | Mitochondria - metabolism | Animals | Oxygen Consumption - genetics | Myositis, Inclusion Body - metabolism | Aged | Nervous system diseases | Neurosciences | Genes | Amyotrophic lateral sclerosis | Genetic aspects | Adenosine triphosphatase | Dementia | Proteins | Medical research | Phosphorylation | Biomedical research | Disease | Rodents | Respiration | Experiments | Patients | Index Medicus | Report
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 3660 - 3663
in this issue of the JCI, two reports provide intriguing new information on the role of the inflammatory cytokine IL-6 in breast and lung cancer. The study by... 
BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | LUNG-CANCER | PATHWAY | STAT3 | NOTCH | STEM/PROGENITOR CELLS | GROWTH-FACTOR | INTERLEUKIN-6 | IDENTIFICATION | TUMORIGENESIS | Receptor, Epidermal Growth Factor - genetics | Transcription, Genetic - drug effects | Interleukin-6 - antagonists & inhibitors | Carbonic Anhydrases - biosynthesis | Cytokine Receptor gp130 - genetics | Receptors, Notch - metabolism | Humans | Lung Neoplasms - metabolism | Antigens, Neoplasm - biosynthesis | Spheroids, Cellular - pathology | Neoplasm Proteins - pharmacology | Receptors, Notch - genetics | Janus Kinases - metabolism | RNA, Messenger - metabolism | Serrate-Jagged Proteins | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Interleukin-6 - metabolism | Gene Expression Regulation, Neoplastic - genetics | STAT3 Transcription Factor - genetics | Cytokine Receptor gp130 - metabolism | Interleukin-6 - genetics | Membrane Proteins - genetics | Spheroids, Cellular - metabolism | Enzyme Inhibitors - pharmacology | Mammary Glands, Human - pathology | Lung Neoplasms - therapy | Signal Transduction - genetics | Autocrine Communication - genetics | Breast Neoplasms - genetics | RNA, Neoplasm - biosynthesis | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | RNA, Neoplasm - genetics | Stem Cells - pathology | Carcinoma - genetics | Mice | Mutation | Transcription, Genetic - genetics | Cell Hypoxia - genetics | Calcium-Binding Proteins - genetics | Neoplasm Transplantation | Carbonic Anhydrases - genetics | Lung Neoplasms - pathology | Autocrine Communication - drug effects | Mammary Glands, Human - metabolism | Neoplasm Proteins - metabolism | Stem Cells - metabolism | Breast Neoplasms - metabolism | Breast Neoplasms - therapy | Intercellular Signaling Peptides and Proteins - metabolism | Receptor, Epidermal Growth Factor - metabolism | Female | Membrane Proteins - metabolism | Gene Expression Regulation, Neoplastic - drug effects | Carcinoma - pathology | STAT3 Transcription Factor - metabolism | Carbonic Anhydrase IX | Calcium-Binding Proteins - metabolism | Lung Neoplasms - genetics | Antigens, Neoplasm - genetics | Cell Hypoxia - drug effects | Janus Kinases - genetics | Neoplasm Invasiveness | RNA, Messenger - genetics | RNA, Small Interfering - pharmacology | Intercellular Signaling Peptides and Proteins - genetics | Up-Regulation - genetics | Up-Regulation - drug effects | Animals | Interleukin-6 - pharmacology | Breast Neoplasms - pathology | Interleukin-6 - biosynthesis | Carcinoma - therapy | Receptor, Notch3 | Carcinoma - metabolism | Antagonists (Biochemistry) | Epithelial tumors | Dosage and administration | Diagnosis | Research | Drug therapy | Health aspects | Interleukin-6 | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 01/2014, Volume 289, Issue 1, pp. 13 - 27
Highly pathogenic avian influenza viruses (HPAIV) induce severe inflammation in poultry and men. One characteristic of HPAIV infections is the induction of a... 
TRANSCRIPTIONAL ACTIVATION | STAT Transcription Factor | MAP KINASE | HUMAN MACROPHAGES | BIOCHEMISTRY & MOLECULAR BIOLOGY | Influenza Virus | STAT Signaling | Highly Pathogenic Avian Influenza Virus (HPAIV) | SERINE PHOSPHORYLATION | p38 MAPK | Endothelium | A VIRUS | Hypercytokinemia | ANTIVIRAL RESPONSES | JAK | SIGNALING PATHWAY | ENDOTHELIAL-CELLS | INTERFERON REGULATORY FACTOR-3 | Interferon | NF-KAPPA-B | Orthomyxoviridae Infections - prevention & control | Humans | Cercopithecus aethiops | Male | Influenza A Virus, H5N1 Subtype - genetics | Orthomyxoviridae Infections - enzymology | Promoter Regions, Genetic - genetics | Orthomyxoviridae Infections - genetics | Phosphorylation - genetics | STAT1 Transcription Factor - metabolism | MAP Kinase Signaling System - genetics | Madin Darby Canine Kidney Cells | Interferon-beta - genetics | Female | p38 Mitogen-Activated Protein Kinases - metabolism | Influenza A Virus, H5N1 Subtype - metabolism | Phosphorylation - drug effects | Cytokines - genetics | Vero Cells | Influenza A Virus, H7N7 Subtype | Gene Expression Regulation - genetics | Orthomyxoviridae Infections - pathology | Enzyme Inhibitors - pharmacology | Interferon-beta - biosynthesis | p38 Mitogen-Activated Protein Kinases - genetics | Imidazoles - pharmacology | STAT1 Transcription Factor - genetics | Gene Expression Regulation - drug effects | Animals | MAP Kinase Signaling System - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Dogs | Mice | Mice, Inbred BALB C | Pyridines - pharmacology | Cytokines - biosynthesis | Index Medicus | Molecular Bases of Disease
Journal Article