Cancer Discovery, ISSN 2159-8274, 06/2018, Volume 8, Issue 6, pp. 714 - 729
The cornerstone of treatment for advanced ALK-positive lung cancer is sequential therapy with increasingly potent and selective ALK inhibitors. The...
EML4-ALK | DRUG-COMBINATIONS | GENE | ONCOLOGY | CERITINIB | OVERCOMES CRIZOTINIB RESISTANCE | ALECTINIB | ACQUIRED-RESISTANCE | OPEN-LABEL | ROS1 | CHEMOTHERAPY | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Lung Neoplasms - chemically induced | Humans | Ethylnitrosourea - adverse effects | Drug Resistance, Neoplasm | Lactams, Macrocyclic - pharmacology | Anaplastic Lymphoma Kinase - genetics | Whole Exome Sequencing | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Animals | Oncogene Proteins, Fusion - genetics | Crizotinib - pharmacology | Cell Line, Tumor | Crizotinib - administration & dosage | Female | Lactams, Macrocyclic - administration & dosage | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Index Medicus | ALK | brigatinib | crizotinib | lorlatinib | and NSCLC | Anaplastic lymphoma kinase | ceritinib | acquired resistance | alectinib
EML4-ALK | DRUG-COMBINATIONS | GENE | ONCOLOGY | CERITINIB | OVERCOMES CRIZOTINIB RESISTANCE | ALECTINIB | ACQUIRED-RESISTANCE | OPEN-LABEL | ROS1 | CHEMOTHERAPY | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Lung Neoplasms - chemically induced | Humans | Ethylnitrosourea - adverse effects | Drug Resistance, Neoplasm | Lactams, Macrocyclic - pharmacology | Anaplastic Lymphoma Kinase - genetics | Whole Exome Sequencing | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Animals | Oncogene Proteins, Fusion - genetics | Crizotinib - pharmacology | Cell Line, Tumor | Crizotinib - administration & dosage | Female | Lactams, Macrocyclic - administration & dosage | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Index Medicus | ALK | brigatinib | crizotinib | lorlatinib | and NSCLC | Anaplastic lymphoma kinase | ceritinib | acquired resistance | alectinib
Journal Article
Cell Reports, ISSN 2211-1247, 12/2017, Volume 21, Issue 11, pp. 3298 - 3309
Personalized cancer therapy is based on a patient’s tumor lineage, histopathology, expression analyses, and/or tumor DNA or RNA analysis. Here, we aim to...
NSCLC | patient-derived cancer cells | personalized medicine | LUNG-CANCER | STEM-CELLS | GEFITINIB | ROCK INHIBITOR | EPITHELIAL-CELLS | MODELS | CERITINIB | RESISTANCE | PRECISION MEDICINE | REPROGRAMMED CELLS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Pyrazoles - therapeutic use | Primary Cell Culture - methods | Humans | Lung Neoplasms - metabolism | ErbB Receptors - genetics | Lung Neoplasms - pathology | Antineoplastic Agents - therapeutic use | Anaplastic Lymphoma Kinase | Neoplasms - genetics | Biomarkers, Tumor - metabolism | Lactams, Macrocyclic - therapeutic use | Tumor Cells, Cultured | Pyridines - therapeutic use | Crizotinib | Lung Neoplasms - genetics | Gene Expression | ErbB Receptors - metabolism | Fluorescent Antibody Technique - methods | Keratin-8 - genetics | Neoplasms - classification | Piperazines - therapeutic use | Receptor Protein-Tyrosine Kinases - metabolism | Keratin-18 - genetics | Neoplasms - drug therapy | High-Throughput Screening Assays | Keratin-8 - metabolism | Receptor Protein-Tyrosine Kinases - genetics | Biopsy | Keratin-18 - metabolism | Feeder Cells - cytology | Biomarkers, Tumor - genetics | Erlotinib Hydrochloride - therapeutic use | Mutation | Neoplasms - pathology | Precision Medicine - methods
NSCLC | patient-derived cancer cells | personalized medicine | LUNG-CANCER | STEM-CELLS | GEFITINIB | ROCK INHIBITOR | EPITHELIAL-CELLS | MODELS | CERITINIB | RESISTANCE | PRECISION MEDICINE | REPROGRAMMED CELLS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Pyrazoles - therapeutic use | Primary Cell Culture - methods | Humans | Lung Neoplasms - metabolism | ErbB Receptors - genetics | Lung Neoplasms - pathology | Antineoplastic Agents - therapeutic use | Anaplastic Lymphoma Kinase | Neoplasms - genetics | Biomarkers, Tumor - metabolism | Lactams, Macrocyclic - therapeutic use | Tumor Cells, Cultured | Pyridines - therapeutic use | Crizotinib | Lung Neoplasms - genetics | Gene Expression | ErbB Receptors - metabolism | Fluorescent Antibody Technique - methods | Keratin-8 - genetics | Neoplasms - classification | Piperazines - therapeutic use | Receptor Protein-Tyrosine Kinases - metabolism | Keratin-18 - genetics | Neoplasms - drug therapy | High-Throughput Screening Assays | Keratin-8 - metabolism | Receptor Protein-Tyrosine Kinases - genetics | Biopsy | Keratin-18 - metabolism | Feeder Cells - cytology | Biomarkers, Tumor - genetics | Erlotinib Hydrochloride - therapeutic use | Mutation | Neoplasms - pathology | Precision Medicine - methods
Journal Article
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Full Text
Targeting FGFR overcomes EMT-mediated resistance in EGFR mutant non-small cell lung cancer
ONCOGENE, ISSN 0950-9232, 09/2019, Volume 38, Issue 37, pp. 6399 - 6413
Evolved resistance to tyrosine kinase inhibitor (TKI)-targeted therapies remains a major clinical challenge. In epidermal growth factor receptor (EGFR) mutant...
MULTIPLE-MYELOMA | GEFITINIB | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | CELL BIOLOGY | TO-MESENCHYMAL TRANSITION | MET AMPLIFICATION | ONCOLOGY | PATHWAY | GENETICS & HEREDITY | GROWTH-FACTOR RECEPTOR-3 | INHIBITOR | ACTIVATING MUTATIONS | Tyrosine | CRISPR | Fibroblast growth factor | Cell survival | Epidermal growth factor receptors | Small cell lung carcinoma | Mesenchyme | Lung cancer | Non-small cell lung carcinoma | Genomes | Gene expression | Drug resistance | Kinases | Epidermal growth factor | Motivation | Cell lines | Growth factors | Fibroblast growth factor receptor 1 | Protein-tyrosine kinase | Fibroblast growth factor receptors
MULTIPLE-MYELOMA | GEFITINIB | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ACQUIRED-RESISTANCE | CELL BIOLOGY | TO-MESENCHYMAL TRANSITION | MET AMPLIFICATION | ONCOLOGY | PATHWAY | GENETICS & HEREDITY | GROWTH-FACTOR RECEPTOR-3 | INHIBITOR | ACTIVATING MUTATIONS | Tyrosine | CRISPR | Fibroblast growth factor | Cell survival | Epidermal growth factor receptors | Small cell lung carcinoma | Mesenchyme | Lung cancer | Non-small cell lung carcinoma | Genomes | Gene expression | Drug resistance | Kinases | Epidermal growth factor | Motivation | Cell lines | Growth factors | Fibroblast growth factor receptor 1 | Protein-tyrosine kinase | Fibroblast growth factor receptors
Journal Article
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