MEK1/2 inhibitor withdrawal reverses acquired resistance driven by BRAF<sup>V600E</sup> amplification whereas KRAS<sup>G13D</sup> amplification promotes EMT-chemoresistance.
第一作者:
Matthew J,Sale
第一单位:
Signalling Programme, The Babraham Institute, Babraham Research Campus, Cambridge, CB22 3AT, UK. matthew.sale@babraham.ac.uk.
作者:
医学主题词
抗肿瘤药(Antineoplastic Agents);细胞凋亡(Apoptosis);苯咪唑类(Benzimidazoles);细胞系, 肿瘤(Cell Line, Tumor);抗药性, 肿瘤(Drug Resistance, Neoplasm);上皮-间质转化(Epithelial-Mesenchymal Transition);女(雌)性(Female);基因扩增(Gene Amplification);基因表达调控, 肿瘤(Gene Expression Regulation, Neoplastic);人类(Humans);MAP激酶激酶1(MAP Kinase Kinase 1);MAP激酶激酶2(MAP Kinase Kinase 2);MAP激酶信号系统(MAP Kinase Signaling System);男(雄)性(Male);丝裂原活化蛋白激酶1(Mitogen-Activated Protein Kinase 1);丝裂原活化蛋白激酶3(Mitogen-Activated Protein Kinase 3);肿瘤(Neoplasms);蛋白激酶抑制剂(Protein Kinase Inhibitors);原癌基因蛋白质B-raf(Proto-Oncogene Proteins B-raf);原癌基因蛋白质类p21(ras)(Proto-Oncogene Proteins p21(ras));停止治疗(Withholding Treatment)
DOI
10.1038/s41467-019-09438-w
PMID
31048689
发布时间
2025-05-30
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