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Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7572, pp. 263 - 267
Colorectal cancer is the third most common cancer worldwide, with 1.2 million patients diagnosed annually. In late-stage colorectal cancer, the most commonly... 
PANITUMUMAB | THERAPY | MULTIDISCIPLINARY SCIENCES | SEQUENCE | ACQUIRED-RESISTANCE | SOMATIC MUTATION | IDENTIFICATION | GENE COPY NUMBER | ACTIVATING MUTATIONS | BREAST | INSIGHTS | Receptor, Epidermal Growth Factor - genetics | Receptor, ErbB-2 - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Colorectal Neoplasms - genetics | Genomics | Humans | Antibodies, Monoclonal - therapeutic use | Antineoplastic Agents - therapeutic use | Cetuximab - therapeutic use | Molecular Targeted Therapy | Receptor, Fibroblast Growth Factor, Type 1 - genetics | MAP Kinase Kinase 1 - genetics | Colorectal Neoplasms - drug therapy | Female | Antineoplastic Agents - pharmacology | Insulin Receptor Substrate Proteins - genetics | Colorectal Neoplasms - metabolism | Antibodies, Monoclonal - pharmacology | Cetuximab - pharmacology | DNA Copy Number Variations - genetics | Mutation - genetics | Genome, Human - genetics | Receptor, Epidermal Growth Factor - chemistry | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Exome - genetics | Animals | Receptor, Platelet-Derived Growth Factor alpha - genetics | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mice | Drug Resistance, Neoplasm - drug effects | Care and treatment | Gene mutations | Colorectal cancer | Drug metabolism | Genetic aspects | Identification and classification | Health aspects | Proteins | Epidermal growth factor | Genes | Clinical trials | Mutation | Kinases | Cancer therapies | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 508, Issue 1, pp. 118 - 122
Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably(1,2).... 
GROWTH-FACTOR RECEPTOR | BRAF INHIBITOR | RAF INHIBITION | CELLS | MULTIDISCIPLINARY SCIENCES | IMPROVED SURVIVAL | DIFFERENTIATION | C-JUN | CANCER | EXPRESSION | EGFR | Receptor, Epidermal Growth Factor - genetics | Humans | Receptor Protein-Tyrosine Kinases - biosynthesis | Cellular Senescence - drug effects | Melanoma - enzymology | Antineoplastic Agents - administration & dosage | Receptor, Platelet-Derived Growth Factor beta - genetics | Indoles - administration & dosage | Mitogen-Activated Protein Kinase Kinases - metabolism | Receptor, Epidermal Growth Factor - metabolism | Flow Cytometry | Melanoma - genetics | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Proto-Oncogene Proteins B-raf - metabolism | Receptor, Platelet-Derived Growth Factor beta - metabolism | Receptor, Epidermal Growth Factor - biosynthesis | Gene Library | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Melanoma - pathology | Receptor Protein-Tyrosine Kinases - metabolism | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Protein Kinase Inhibitors - administration & dosage | Transforming Growth Factor beta - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Receptor Protein-Tyrosine Kinases - genetics | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Transforming Growth Factor beta - metabolism | Receptor, Platelet-Derived Growth Factor beta - biosynthesis | Sulfonamides - administration & dosage | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Proteins | Biopsy | Rodents | Genes | Melanoma | Mutation | Kinases | Drug resistance | Patients | Tumors | 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 | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 11/2014, Volume 111, Issue 45, pp. E4869 - E4877
The human FGF receptors (FGFRs) play critical roles in various human cancers, and several FGFR inhibitors are currently under clinical investigation.... 
Structure-based drug design | Drug discovery | Cancer drug resistance | Kinase inhibitor | structure-based drug design | WILD-TYPE | MULTIDISCIPLINARY SCIENCES | BCR-ABL | GROWTH-FACTOR RECEPTORS | DRUG-RESISTANCE | kinase inhibitor | LUNG-CANCER | GENE FUSIONS | cancer drug resistance | SELECTIVE INHIBITOR | drug discovery | THERAPEUTIC TARGET | FACTOR RECEPTOR 4 | REGULATES PROLIFERATION | Receptor, Fibroblast Growth Factor, Type 4 - chemistry | Receptor, Epidermal Growth Factor - genetics | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Receptor, Fibroblast Growth Factor, Type 2 - chemistry | Receptor, Fibroblast Growth Factor, Type 2 - metabolism | Humans | Receptor, Fibroblast Growth Factor, Type 1 - metabolism | Crystallography, X-Ray | Structure-Activity Relationship | Mutation, Missense | Receptor, Fibroblast Growth Factor, Type 1 - genetics | Protein Kinase Inhibitors - chemistry | Receptor, Epidermal Growth Factor - metabolism | Neoplasms - genetics | Receptor, Fibroblast Growth Factor, Type 2 - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Binding Sites | Neoplasms - enzymology | Antineoplastic Agents - chemistry | Receptor, Fibroblast Growth Factor, Type 1 - antagonists & inhibitors | Receptor, Epidermal Growth Factor - chemistry | Neoplasms - drug therapy | Drug Resistance, Neoplasm - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Receptor, Fibroblast Growth Factor, Type 1 - chemistry | Neoplasms - pathology | Receptor, Fibroblast Growth Factor, Type 4 - antagonists & inhibitors | Receptor, Fibroblast Growth Factor, Type 2 - genetics | Amino Acid Substitution | Drug Resistance, Neoplasm - drug effects | Amino acids | T cell receptors | Mutation | Kinases | Binding sites | Adenosine triphosphatase | Index Medicus | Biological Sciences | PNAS Plus
Journal Article
Nature Medicine, ISSN 1078-8956, 03/2016, Volume 22, Issue 3, pp. 262 - 269
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
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
PLoS Genetics, ISSN 1553-7390, 06/2008, Volume 4, Issue 6, pp. e1000116 - e1000116
Journal Article