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Journal of Clinical Investigation, ISSN 0021-9738, 07/2008, Volume 118, Issue 7, pp. 2609 - 2619
Journal Article
Oncogene, ISSN 0950-9232, 03/2018, Volume 37, Issue 13, pp. 1775 - 1787
BRAF is one of the most frequently mutated genes across a number of different cancers, with the best-characterized mutation being V600E. Despite the successes... 
WILD-TYPE | FEEDBACK ACTIVATION | COLORECTAL CANCERS | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-RAF | SENSITIVITY | OPEN-LABEL | CELL BIOLOGY | MEK INHIBITION | ONCOLOGY | GENETICS & HEREDITY | B-RAF | MUTATIONS | PHASE-2 TRIAL | Glutamic Acid - genetics | Humans | Lung Neoplasms - metabolism | Receptor Protein-Tyrosine Kinases - physiology | Lung Neoplasms - pathology | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | MAP Kinase Signaling System - genetics | Pyrimidinones - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Tumor Cells, Cultured | Lung Neoplasms - genetics | Mutant Proteins - genetics | Signal Transduction - genetics | HT29 Cells | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Mice, Nude | Proto-Oncogene Proteins B-raf - genetics | Valine - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Pyridones - pharmacology | Amino Acid Substitution | Tyrosine | Phosphorylation | Epidermal growth factor receptors | Lung cancer | Genes | MEK inhibitors | Extracellular signal-regulated kinase | MAP kinase | Raf protein | Kinases | Signal transduction | Protein-tyrosine kinase receptors | Mutation | Protein-tyrosine kinase | Fibroblast growth factor receptors | Tumors
Journal Article
CLINICAL CANCER RESEARCH, ISSN 1078-0432, 05/2013, Volume 19, Issue 10, pp. 2688 - 2698
Journal Article
Clinical Cancer Research, ISSN 1078-0432, 03/2019, Volume 25, Issue 5, pp. 1664 - 1675
PURPOSEIt was recently demonstrated that the EWSR1-FLI1 t(11;22)(q24;12) translocation contributes to the hypersensitivity of Ewing sarcoma to PARP inhibitors,... 
Journal Article
Journal of Thoracic Disease, ISSN 2072-1439, 09/2019, Volume 11, Issue S15, pp. S1844 - S1846
Journal Article
Nature Medicine, ISSN 1078-8956, 03/2016, Volume 22, Issue 3, pp. 262 - 269
Journal Article
Clinical cancer research : an official journal of the American Association for Cancer Research, ISSN 1078-0432, 10/2018
It was recently demonstrated that the translocation contributes to the hypersensitivity of Ewing sarcoma to PARP inhibitors, prompting clinical evaluation of... 
Journal Article
Molecular & Cellular Oncology, 07/2018, Volume 5, Issue 4
Pharmaceutical inhibition of the Human Epidermal growth factor Receptor 2 (HER2) oncogene has dramatically improved outcomes in HER2-amplified breast cancers.... 
MCL1 inhibitor | apoptosis | Breast cancer | miR-4728 | NOXA
Journal Article
Cancer Research, ISSN 0008-5472, 10/2014, Volume 74, Issue 19 Supplement, pp. 2933 - 2933
Journal Article
Translational Cancer Research, ISSN 2218-676X, 08/2018, Volume 7, Issue S7, pp. S787 - S791
Journal Article
Molecular Cancer Research, ISSN 1541-7786, 10/2013, Volume 11, Issue 10 Supplement, pp. A062 - A062
Journal Article
Cancer Science, ISSN 1347-9032, 05/2014, Volume 105, Issue 5, pp. 499 - 505
Mutations in Kirsten rat‐sarcoma (KRAS) are well appreciated to be major drivers of human cancers through dysregulation of multiple growth and survival... 
Proteins | Sarcoma | Lung cancer | Lethality | Tumorigenesis | Mutation | Kinases | Growth factors | Survival | Tumors
Journal Article
JOURNAL OF CLINICAL INVESTIGATION, ISSN 0021-9738, 07/2008, Volume 118, Issue 7, pp. 2609 - 2619
Although some cancers are initially sensitive to EGFR tyrosine kinase inhibitors (TKIs), resistance invariably develops. We investigated mechanisms of acquired... 
BREAST-CANCER | GENE-MUTATIONS | MEDICINE, RESEARCH & EXPERIMENTAL | LUNG-CANCER | GROWTH-FACTOR-RECEPTOR | T790M MUTATIONS | IN-VIVO | TUMOR-CELLS | ANTITUMOR-ACTIVITY | GEFITINIB SENSITIVITY | ERLOTINIB | Insulin-Like Growth Factor Binding Protein 3 - genetics | Receptor, IGF Type 1 - metabolism | Insulin-Like Growth Factor I - pharmacology | Receptor, ErbB-3 - metabolism | Receptor, IGF Type 1 - antagonists & inhibitors | Gene Expression - drug effects | Carcinoma, Squamous Cell - pathology | Humans | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Insulin-Like Growth Factor Binding Protein 3 - metabolism | Insulin Receptor Substrate Proteins | Insulin-Like Growth Factor Binding Protein 4 - metabolism | Female | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Cell Survival - drug effects | Insulin-Like Growth Factor Binding Proteins - genetics | Insulin-Like Growth Factor Binding Protein 4 - genetics | Insulin-Like Growth Factor II - metabolism | Insulin-Like Growth Factor Binding Proteins - metabolism | Xenograft Model Antitumor Assays | Animals | Carcinoma, Squamous Cell - drug therapy | Mice, Nude | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Mice | Protein Kinase Inhibitors - pharmacology | Adaptor Proteins, Signal Transducing - metabolism | Quinazolines - pharmacology | Insulin-Like Growth Factor I - metabolism | Tyrosine | Phenols | Binding proteins | Analysis | Cancer cells
Journal Article
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
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2013, Volume 110, Issue 52, pp. 21124 - 21129
Journal Article
Cancer Cell, ISSN 1535-6108, 01/2013, Volume 23, Issue 1, pp. 121 - 128
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2013, Volume 110, Issue 52, p. 21124
  The PI3K pathway is genetically altered in excess of 70% of breast cancers, largely through PIK3CA mutation and HER2 amplification. Preclinical studies have... 
Phosphorylation | Biomarkers | Genetics | Breast cancer | Mutation | Kinases | Apoptosis
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2009, Volume 106, Issue 46, pp. 19503 - 19508
Non-small cell lung cancers with activating mutations in the epidermal growth factor receptor (EGFR) are highly responsive to EGFR tyrosine kinase inhibitors... 
B lymphocytes | Cell death | Cell lines | Breast cancer | Down regulation | Genetic mutation | Apoptosis | Lung neoplasms | Cancer | Tumors | Mcl-1 | MEK | AKT | Acquired resistance | BIM | GEFITINIB | GROWTH-FACTOR-RECEPTOR | MULTIDISCIPLINARY SCIENCES | ACQUIRED-RESISTANCE | ANTITUMOR-ACTIVITY | PHOSPHATIDYLINOSITOL 3-KINASE/MAMMALIAN TARGET | acquired resistance | CELL LUNG-CANCER | TYROSINE KINASE INHIBITORS | PATHWAY | T790M MUTATIONS | RAPAMYCIN INHIBITOR | Erlotinib Hydrochloride | Protein Kinases - metabolism | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Receptor, ErbB-2 - genetics | Humans | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Quinolines - pharmacology | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Lung Neoplasms - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Antineoplastic Combined Chemotherapy Protocols | Imidazoles - pharmacology | Breast Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - genetics | Protein Kinase Inhibitors - therapeutic use | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | Carcinoma, Non-Small-Cell Lung - drug therapy | Quinazolines - pharmacology | Physiological aspects | Research | Lung cancer, Non-small cell | Phosphotransferases | Health aspects | Biological Sciences
Journal Article