Amplification of the driving oncogene, KRAS or BRAF, underpins acquired resistance to MEK1/2 inhibitors in colorectal cancer cells.
第一作者:
Annette S,Little
第一单位:
Laboratory of Molecular Signalling, Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK. annette.little@bbsrc.ac.uk
作者:
医学主题词
氨基酸取代(Amino Acid Substitution);苯咪唑类(Benzimidazoles);细胞系, 肿瘤(Cell Line, Tumor);结直肠肿瘤(Colorectal Neoplasms);抗药性, 肿瘤(Drug Resistance, Neoplasm);基因扩增(Gene Amplification);基因表达调控, 酶学(Gene Expression Regulation, Enzymologic);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);突变, 误义(Mutation, Missense);蛋白激酶抑制剂(Protein Kinase Inhibitors);原癌基因蛋白质类(Proto-Oncogene Proteins);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));ras蛋白质类(ras Proteins)
DOI
10.1126/scisignal.2001752
PMID
21447798
发布时间
2025-05-29
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Science signaling
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