Wild-type and mutated IDH1/2 enzymes and therapy responses

被引：175
作者：
Molenaar, Remco J. [1 ,2 ,3 ]
Maciejewski, Jaroslaw P. [3 ]
Wilmink, Johanna W. [2 ]
van Noorden, Cornelis J. F. [1 ]
机构：
[1] Acad Med Ctr, Canc Ctr Amsterdam, Dept Med Biol, Amsterdam, Netherlands
[2] Acad Med Ctr, Canc Ctr Amsterdam, Dept Med Oncol, Amsterdam, Netherlands
[3] Cleveland Clin, Dept Translat Hematol & Oncol Res, Cleveland, OH 44106 USA
来源：
ONCOGENE | 2018年 / 37卷 / 15期
基金：
美国国家卫生研究院;
关键词：
ACUTE MYELOID-LEUKEMIA; ISOCITRATE DEHYDROGENASE 1; PREDICT LONGER SURVIVAL; DNA-REPAIR ENZYMES; LOW-GRADE GLIOMAS; MUTANT IDH1; INTRAHEPATIC CHOLANGIOCARCINOMA; OXIDATIVE STRESS; TUMOR-CELLS; IN-VIVO;
D O I：
10.1038/s41388-017-0077-z
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Isocitrate dehydrogenase 1 and 2 (IDH1/2) are key enzymes in cellular metabolism, epigenetic regulation, redox states, and DNA repair. IDH1/2 mutations are causal in the development and/or progression of various types of cancer due to supraphysiological production of D-2-hydroxyglutarate. In various tumor types, IDH1/2-mutated cancers predict for improved responses to treatment with irradiation or chemotherapy. The present review discusses the molecular basis of the sensitivity of IDH1/2-mutated cancers with respect to the function of mutated IDH1/2 in cellular processes and their interactions with novel IDH1/2-mutant inhibitors. Finally, lessons learned from IDH1/2 mutations for future clinical applications in IDH1/2 wild-type cancers are discussed.
引用
收藏
页码：1949 / 1960
页数：12
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