Long-term vemurafenib treatment drives inhibitor resistance through a spontaneous KRAS G12D mutation in a BRAF V600E papillary thyroid carcinoma model. [electronic resource]
Producer: 20171229Description: 30907-23 p. digitalISSN:- 1949-2553
- Aged
- Antineoplastic Agents -- pharmacology
- Benzimidazoles -- pharmacology
- Carcinoma, Papillary -- drug therapy
- Cell Line, Tumor
- Drug Resistance, Neoplasm -- genetics
- Enzyme Inhibitors -- pharmacology
- ErbB Receptors -- metabolism
- Female
- Gain of Function Mutation
- Gene Knockdown Techniques
- Heterocyclic Compounds, 3-Ring -- pharmacology
- Humans
- Indoles -- pharmacology
- MAP Kinase Kinase 1 -- antagonists & inhibitors
- MAP Kinase Signaling System
- Male
- Mitogen-Activated Protein Kinase 1 -- antagonists & inhibitors
- Mitogen-Activated Protein Kinase 3 -- antagonists & inhibitors
- Proto-Oncogene Proteins B-raf -- genetics
- Proto-Oncogene Proteins c-akt -- antagonists & inhibitors
- Proto-Oncogene Proteins p21(ras) -- genetics
- Pyridones -- pharmacology
- Pyrimidines -- pharmacology
- RNA Interference
- RNA, Small Interfering
- Sulfonamides -- pharmacology
- Thyroid Cancer, Papillary
- Thyroid Neoplasms -- drug therapy
- Vemurafenib
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Publication Type: Journal Article
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