Epithelial-mesenchymal transition (EMT) beyond EGFR mutations per se is a common mechanism for acquired resistance to EGFR TKI. [electronic resource]
Producer: 20190508Description: 455-468 p. digitalISSN:- 1476-5594
- Acrylamides
- Aniline Compounds
- Animals
- Antigens, CD -- biosynthesis
- Antineoplastic Agents -- pharmacology
- Cadherins -- antagonists & inhibitors
- Carcinoma, Non-Small-Cell Lung -- drug therapy
- Cell Line, Tumor
- Drug Resistance, Neoplasm -- genetics
- Drug Screening Assays, Antitumor
- Epithelial-Mesenchymal Transition -- drug effects
- ErbB Receptors -- genetics
- Gefitinib -- pharmacology
- Gene Expression Regulation, Neoplastic -- drug effects
- Histone Deacetylase Inhibitors -- pharmacology
- Humans
- Hydroxymethylglutaryl-CoA Reductase Inhibitors -- pharmacology
- Lung Neoplasms -- drug therapy
- Mice
- Mice, Inbred BALB C
- Mice, Nude
- Neoplasm Proteins -- antagonists & inhibitors
- Neoplastic Stem Cells -- drug effects
- Piperazines -- pharmacology
- Protein Kinase Inhibitors -- pharmacology
- RNA Interference
- RNA, Small Interfering -- pharmacology
- Specific Pathogen-Free Organisms
- Ubiquitin-Protein Ligases -- antagonists & inhibitors
- Vimentin -- antagonists & inhibitors
- Zinc Finger E-box-Binding Homeobox 1 -- biosynthesis
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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