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Science, ISSN 0036-8075, 12/2014, Volume 346, Issue 6216, pp. 1480 - 1486
Targeted cancer therapies have produced substantial clinical responses, but most tumors develop resistance to these drugs. Here, we describe a pharmacogenomic... 
CELL LUNG-CANCER | ALK | KINASE INHIBITION | GEFITINIB | ACTIVATION | CERITINIB | MULTIDISCIPLINARY SCIENCES | CRIZOTINIB | MUTATIONS | CHEMOTHERAPY | BYPASS MECHANISMS | Lung Neoplasms - drug therapy | Sulfones - therapeutic use | Humans | Receptor, Fibroblast Growth Factor, Type 3 - antagonists & inhibitors | MAP Kinase Kinase 1 - genetics | DNA Mutational Analysis | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Tumor Cells, Cultured | Molecular Targeted Therapy - methods | Lung Neoplasms - genetics | Receptor, Fibroblast Growth Factor, Type 3 - genetics | Lung Neoplasms - enzymology | Carcinoma, Non-Small-Cell Lung - genetics | MAP Kinase Kinase 1 - metabolism | Proto-Oncogene Proteins pp60(c-src) - antagonists & inhibitors | Patient-Specific Modeling | Drug Resistance, Neoplasm - genetics | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Mutation | Enzyme Activation - genetics | Drug Screening Assays, Antitumor | Antimitotic agents | Cancer patients | Care and treatment | Lung cancer | Dosage and administration | Genetic aspects | Antineoplastic agents | Drug therapy | Drug resistance | Methods | Cancer | Cell culture | Oncology | Pharmaceutical sciences | Drugs | Mutations | Therapy | Genetics | Kinases | Patients | Tumors
Journal Article
Nucleic Acids Research, ISSN 0305-1048, 5/2009, Volume 37, Issue 9, pp. 2882 - 2893
Journal Article
Nature, ISSN 0028-0836, 12/2015, Volume 528, Issue 7580, pp. 84 - 87
Large cancer cell line collections broadly capture the genomic diversity of human cancers and provide valuable insight into anti-cancer drug response. Here we... 
DRUG-SENSITIVITY | MULTIDISCIPLINARY SCIENCES | Pharmacogenetics | Reproducibility of Results | Datasets as Topic | Neoplasms - genetics | Humans | Inhibitory Concentration 50 | Cell Line, Tumor - drug effects | Neoplasms - pathology | Databases, Factual | Neoplasms - drug therapy | Drugs | Studies | Datasets | Correlation analysis | Genomics | Pharmacology | Cancer
Journal Article
Modern Pathology, ISSN 0893-3952, 2019, Volume 32, Issue 6, pp. 844 - 854
Metastasis following surgical resection is a leading cause of mortality in pancreatic ductal adenocarcinoma. Epithelial-mesenchymal transition is thought to... 
CELLS | TO-MESENCHYMAL TRANSITION | SUBTYPES | BIOLOGY | TUMOR | MYOFIBROBLASTS | PATHOLOGY | EMT | EXPRESSION | FAILURE | PLASTICITY | Immunohistochemistry | Adenocarcinoma | Phenotypes | Mesenchyme | DNA probes | Tumor cells | Colorimetry | Metastasis | Hybridization | Ribonucleic acid--RNA | Smad4 protein | Metastases | Genotype & phenotype | RNA probes | Pancreas | Tumors
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2015, Volume 10, Issue 10, p. e0140310
A newer generation of anti-cancer drugs targeting underlying somatic genetic driver events have resulted in high single-agent or single-pathway response rates... 
RAF INHIBITION | MEK | PATHWAY | MULTIDISCIPLINARY SCIENCES | GROWTH | ACQUIRED-RESISTANCE | TYROSINE KINASE INHIBITOR | CANCER | CONFERS RESISTANCE | Humans | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Receptors, Vascular Endothelial Growth Factor - metabolism | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Cell Death - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Receptors, Platelet-Derived Growth Factor - antagonists & inhibitors | Melanoma - pathology | Sulfonamides - pharmacology | Drug Synergism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | High-Throughput Screening Assays | Sulfonamides - therapeutic use | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Quinazolines - therapeutic use | Receptors, Platelet-Derived Growth Factor - metabolism | Melanoma - drug therapy | ATP Binding Cassette Transporter, Sub-Family B - metabolism | Cell Line, Tumor | Indoles - therapeutic use | Mice | Quinazolines - pharmacology | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Patient outcomes | Melanoma | Development and progression | Dosage and administration | Research | Drug resistance | Antineoplastic agents | Drug therapy | Vascular endothelial growth factor | Drugs | Biotechnology | Animal models | Genomics | Clinical trials | Oncology | Biology | Drug delivery | Metastasis | Kinases | Cancer therapies | Medical schools | Mammalian cells | Skin cancer | MDR1 protein | Signal transduction | Cell cycle | Protein transport | P-Glycoprotein | Tyrosine | Sensitizing | Dermatology | Multidrug resistance | MAP kinase | Regression analysis | Gene expression | Patients | Vascular endothelial growth factor receptors | Hospitals | Inhibitors | Protein kinase | Biopsy | Cell lines | Mutation | Transporter | Apoptosis | Cancer
Journal Article
Cell Reports, ISSN 2211-1247, 02/2018, Volume 22, Issue 7, pp. 1889 - 1902
KRAS can bind numerous effector proteins, which activate different downstream signaling events. The best known are RAF, phosphatidylinositide (PI)-3′ kinase,... 
RNAi screen | KRAS | RSK | redundancy | paralogs | TO-MESENCHYMAL TRANSITION | INHIBITION | CELL-MIGRATION | ADENOCARCINOMA | PROLIFERATION | REGULATORS | IDENTIFICATION | MUTANT LUNG-CANCER | REQUIREMENT | REVEALS | CELL BIOLOGY
Journal Article