Met gene amplification and protein hyperactivation is a mechanism of resistance to both first and third generation EGFR inhibitors in lung cancer treatment. [electronic resource]
Producer: 20170728Description: 494-504 p. digitalISSN:- 1872-7980
- Acrylamides -- pharmacology
- Aniline Compounds -- pharmacology
- Animals
- Antineoplastic Agents -- pharmacology
- Antineoplastic Combined Chemotherapy Protocols -- pharmacology
- Apoptosis -- drug effects
- Carcinoma, Non-Small-Cell Lung -- drug therapy
- Cell Line, Tumor
- Cell Proliferation -- drug effects
- Crizotinib
- Dose-Response Relationship, Drug
- Drug Resistance, Neoplasm -- drug effects
- ErbB Receptors -- antagonists & inhibitors
- Erlotinib Hydrochloride -- pharmacology
- Female
- G1 Phase Cell Cycle Checkpoints -- drug effects
- Gene Amplification
- Gene Expression Regulation, Neoplastic
- Humans
- Lung Neoplasms -- drug therapy
- Mice, Nude
- Molecular Targeted Therapy
- Mutation
- Protein Kinase Inhibitors -- pharmacology
- Proto-Oncogene Proteins c-met -- genetics
- Pyrazoles -- pharmacology
- Pyridines -- pharmacology
- Pyrimidines -- pharmacology
- RNA Interference
- Signal Transduction -- drug effects
- Time Factors
- Transfection
- Tumor Burden -- drug effects
- Xenograft Model Antitumor Assays
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Publication Type: Journal Article
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