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Cancer, ISSN 0008-543X, 10/2014, Volume 120, Issue 19, pp. 2980 - 2985
BACKGROUND Targeting a single pathway in pancreatic adenocarcinoma (PC) is unlikely to affect its natural history. We tested the hypothesis that simulataneous... 
pancreatic cancer | erlotinib signaling | randomized phase II | IGF‐1R | cixutumumab | EGFR | targeted treatment | Erlotinib signaling | Targeted treatment | Randomized phase II | Pancreatic cancer | Cixutumumab | IGF-1R | CARCINOMA-CELLS | DUCTAL ADENOCARCINOMA | MONOCLONAL-ANTIBODY | SINGLE-AGENT CETUXIMAB | BREAST-CANCER | INHIBITION | K-RAS | ONCOLOGY | THERAPEUTIC TARGET | C-MET | RESISTANCE | Erlotinib Hydrochloride | Pancreatic Neoplasms - metabolism | Humans | Middle Aged | Antibodies, Monoclonal - adverse effects | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Receptor, Epidermal Growth Factor - drug effects | Male | Insulin-Like Growth Factor I - drug effects | Pancreatic Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - metabolism | Adenocarcinoma - metabolism | Adult | Deoxycytidine - adverse effects | Female | Quinazolines - administration & dosage | Drug Administration Schedule | Deoxycytidine - administration & dosage | Pancreatic Neoplasms - pathology | Kaplan-Meier Estimate | Treatment Outcome | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Disease-Free Survival | Signal Transduction - drug effects | Antibodies, Monoclonal - administration & dosage | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Quinazolines - adverse effects | Aged | Deoxycytidine - analogs & derivatives | Insulin-Like Growth Factor I - metabolism | Index Medicus | Abridged Index Medicus
Journal Article
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
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2013, Volume 8, Issue 3, p. e60317
Aberrant expression of microRNA-146a (miR-146a) has been reported to be involved in the development and progression of various types of cancers. However, its... 
SUPPRESSOR | ONCOGENESIS | RNA | MULTIDISCIPLINARY SCIENCES | CERVICAL-CANCER | INTERFERENCE | MICRORNAS | NF-KAPPA-B | FACTOR RECEPTOR | EXPRESSION | CONTRIBUTES | Lung Neoplasms - drug therapy | Humans | Lung Neoplasms - metabolism | Middle Aged | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Male | MicroRNAs - metabolism | NF-kappa B - metabolism | Receptor, Epidermal Growth Factor - metabolism | Antibodies, Monoclonal, Humanized - pharmacology | Aged, 80 and over | Adult | Female | Antineoplastic Agents - pharmacology | Lung - metabolism | Cetuximab | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Lung - pathology | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Lung - drug effects | Cell Line, Tumor | Aged | Cell Proliferation - drug effects | MicroRNAs - genetics | Carcinoma, Non-Small-Cell Lung - drug therapy | Apoptosis | Cell Movement | MicroRNA | Growth | Monoclonal antibodies | Lung cancer, Small cell | Development and progression | Lung cancer, Non-small cell | Health aspects | Cell proliferation | Laboratories | Lung cancer | Oncology | Drug delivery | Kinases | Paraffin | Cancer therapies | Metastases | Signal transduction | Cell growth | Bioindicators | Inhibition | Gefitinib | Sensitizing | NF-κB protein | Phenotypes | Cytokines | Epidermal growth factor receptors | MiRNA | Non-small cell lung carcinoma | siRNA | Breast cancer | Gene expression | Ribonucleic acid--RNA | Patients | Pathology | Signaling | Chemotherapy | Thyroid cancer | MicroRNAs | Medical prognosis | Pancreatic cancer | Cell lines | Biomarkers | Mutation | Cell migration | Cervical cancer | Tumors | Cancer | Ribonucleic acid
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 3/2004, Volume 164, Issue 5, pp. 769 - 779
All ligands of the epidermal growth factor receptor (EGFR), which has important roles in development and disease, are released from the membrane by proteases.... 
EGF receptor | Growth factor signaling | EGF receptor ligands | ADAMs | Ectodomain shedding | CELLS | ectodomain shedding | HB-EGF | TACE | PROTEIN-COUPLED RECEPTORS | ALPHA-CONVERTING-ENZYME | growth factor signaling | MICE LACKING | FAMILY | CELL BIOLOGY | EPIDERMAL-GROWTH-FACTOR | TGF-ALPHA | METALLOPROTEASE-DISINTEGRIN | ADAM17 Protein | Metalloendopeptidases - genetics | Phenylalanine - analogs & derivatives | Glycoproteins - metabolism | Metalloendopeptidases - metabolism | Thiophenes - metabolism | Epiregulin | Amphiregulin | Disintegrins - genetics | ADAM12 Protein | Intercellular Signaling Peptides and Proteins - metabolism | Receptor, Epidermal Growth Factor - metabolism | EGF Family of Proteins | Embryo, Mammalian - anatomy & histology | Aspartic Acid Endopeptidases | Amyloid Precursor Protein Secretases | Muscle Proteins - metabolism | Membrane Proteins - metabolism | Transforming Growth Factor alpha - metabolism | Fibroblasts - metabolism | Tetradecanoylphorbol Acetate - metabolism | Protein Structure, Tertiary | Endopeptidases - metabolism | Phenylalanine - metabolism | Disintegrins - metabolism | Membrane Proteins - genetics | Cells, Cultured | Epidermal Growth Factor - metabolism | Genotype | Protease Inhibitors - metabolism | ADAM Proteins | Mice, Knockout | Muscle Proteins - genetics | Heparin-binding EGF-like Growth Factor | Animals | Endopeptidases - genetics | Betacellulin | Ligands | Fibroblasts - cytology | Mice | Cytology | Research | EGF receptor; EGF receptor ligands; ADAMs; ectodomain shedding; growth factor signaling
Journal Article
Placenta, ISSN 0143-4004, 2014, Volume 36, Issue 3, pp. 270 - 278
Abstract Introduction The epidermal growth factor (EGF) signaling system regulates trophoblast differentiation, and its disruption could contribute to... 
Internal Medicine | Obstetrics and Gynecology | Epidermal growth factors | Preeclampsia | Placenta | CELLS | OXIDATIVE STRESS | CYTOTROPHOBLASTS | EGF | HUMAN-PLACENTA | TROPHOBLAST APOPTOSIS | DEVELOPMENTAL BIOLOGY | FACTOR RECEPTOR | OBSTETRICS & GYNECOLOGY | RETARDATION | REPRODUCTIVE BIOLOGY | EARLY-PREGNANCY | ENDOMETRIAL | Receptor, Epidermal Growth Factor - genetics | Humans | Trophoblasts - pathology | Young Adult | Receptor, Epidermal Growth Factor - metabolism | Protein Isoforms - metabolism | Protein Isoforms - chemistry | Transforming Growth Factor alpha - blood | Epidermal Growth Factor - chemistry | Heparin-binding EGF-like Growth Factor - blood | Peptide Fragments - blood | Adult | Female | Pre-Eclampsia - metabolism | Transforming Growth Factor alpha - metabolism | Peptide Fragments - metabolism | Trophoblasts - metabolism | Placentation | Down-Regulation | Epidermal Growth Factor - metabolism | Chorionic Villi - metabolism | Pre-Eclampsia - pathology | Epidermal Growth Factor - blood | Receptor, Epidermal Growth Factor - chemistry | Heparin-binding EGF-like Growth Factor - metabolism | Placenta - metabolism | Pregnancy | Chorionic Villi - pathology | Pre-Eclampsia - blood | Placenta - pathology | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Cell Line, Transformed | Apoptosis | Cohort Studies | Protein Isoforms - genetics | Physiological aspects | Medical colleges | Epidermal growth factor | Cells | placenta | epidermal growth factors | preeclampsia
Journal Article
Molecular Cell, ISSN 1097-2765, 12/2012, Volume 48, Issue 5, pp. 771 - 784
Many types of human tumor cells have overexpressed pyruvate kinase M2 (PKM2). However, the mechanism underlying this increased PKM2 expression remains to be... 
GROWTH-FACTOR RECEPTOR | PROTEIN-KINASE-C | PYRUVATE-KINASE | UBIQUITIN LIGASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ALPHA | BETA-CATENIN | TUMOR-GROWTH | TRANSCRIPTIONAL REGULATION | CANCER | CELL BIOLOGY | Receptor, Epidermal Growth Factor - genetics | Up-Regulation | Glioblastoma - enzymology | Humans | NF-kappa B - metabolism | Ubiquitination | Glioblastoma - genetics | RNA Interference | Cell Transformation, Neoplastic - genetics | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Signal Transduction | Membrane Proteins - genetics | Lactic Acid - metabolism | Protein Kinase C-epsilon - genetics | Brain Neoplasms - genetics | Polypyrimidine Tract-Binding Protein - metabolism | Mice, Nude | Glioblastoma - pathology | Protein Kinase C-epsilon - metabolism | Cell Line, Tumor | Glucose - metabolism | Mice | Enzyme Activation | Mutation | Neoplasm Transplantation | Phosphorylation | Prognosis | Serine | Brain Neoplasms - pathology | Gene Expression Regulation, Neoplastic | Receptor, Epidermal Growth Factor - metabolism | Neoplasm Grading | Transfection | I-kappa B Kinase - metabolism | HEK293 Cells | Female | Membrane Proteins - metabolism | Genes, Reporter | Promoter Regions, Genetic | Brain Neoplasms - enzymology | Phospholipase C gamma - metabolism | Mutagenesis, Site-Directed | Heterogeneous-Nuclear Ribonucleoproteins - metabolism | Epidermal Growth Factor - metabolism | Thyroid Hormones - genetics | Cell Transformation, Neoplastic - metabolism | Gene Expression Regulation, Enzymologic | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | NF-kappa B - genetics | Transcription Factor RelA - metabolism | Thyroid Hormones - metabolism | Glycolysis | Cell Transformation, Neoplastic - pathology
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