Inhibiting Tankyrases sensitizes KRAS-mutant cancer cells to MEK inhibitors via FGFR2 feedback signaling.
第一作者:
Marie,Schoumacher
第一单位:
Authors' Affiliations: Oncology Department, Novartis Institutes for BioMedical Research; Zalicus Inc., Cambridge; and Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts.
作者:
主题词
乙酰胺类(Acetamides);氨基吡啶类(Aminopyridines);苯胺化合物(Aniline Compounds);动物(Animals);抗肿瘤联合化疗方案(Antineoplastic Combined Chemotherapy Protocols);细胞系, 肿瘤(Cell Line, Tumor);药物协同作用(Drug Synergism);反馈, 生理(Feedback, Physiological);女(雌)性(Female);人类(Humans);MAP激酶激酶激酶类(MAP Kinase Kinase Kinases);小鼠(Mice);小鼠, 裸(Mice, Nude);吗啉类(Morpholines);突变(Mutation);蛋白激酶抑制剂(Protein Kinase Inhibitors);原癌基因蛋白质类(Proto-Oncogene Proteins);原癌基因蛋白质类p21(ras)(Proto-Oncogene Proteins p21(ras));嘧啶酮类(Pyrimidinones);喹唑啉类(Quinazolines);受体, 成纤维细胞生长因子, 2型(Receptor, Fibroblast Growth Factor, Type 2);信号传导(Signal Transduction);磺胺类(Sulfonamides);端锚聚合酶类(Tankyrases);噻唑类(Thiazoles);异种移植模型抗肿瘤试验(Xenograft Model Antitumor Assays);ras蛋白质类(ras Proteins)
DOI
10.1158/0008-5472.CAN-14-0138-T
PMID
24747911
发布时间
2019-08-29
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Cancer research
3294-305页
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