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.
Description
Wild-type and mutated IDH1/2 enzymes and therapy responses | Oncogene
%0 Journal Article
%1 molenaar2018wildtype
%A Molenaar, Remco J.
%A Maciejewski, Jaroslaw P.
%A Wilmink, Johanna W.
%A van Noorden, Cornelis J. F.
%D 2018
%J Oncogene
%K IDH1 IDH2 MUSTREAD cancer-research therapeutic-impact therapy wired
%N 15
%P 1949--1960
%R 10.1038/s41388-017-0077-z
%T Wild-type and mutated IDH1/2 enzymes and therapy responses
%U https://doi.org/10.1038/s41388-017-0077-z
%V 37
%X 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.
@article{molenaar2018wildtype,
abstract = {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.},
added-at = {2018-12-07T18:05:16.000+0100},
author = {Molenaar, Remco J. and Maciejewski, Jaroslaw P. and Wilmink, Johanna W. and van Noorden, Cornelis J. F.},
biburl = {https://www.bibsonomy.org/bibtex/29259750985a9972c88d2408ef941bae4/marcsaric},
description = {Wild-type and mutated IDH1/2 enzymes and therapy responses | Oncogene},
doi = {10.1038/s41388-017-0077-z},
interhash = {32c24b05a227f19dba2f280a0dc95ad5},
intrahash = {9259750985a9972c88d2408ef941bae4},
issn = {14765594},
journal = {Oncogene},
keywords = {IDH1 IDH2 MUSTREAD cancer-research therapeutic-impact therapy wired},
number = 15,
pages = {1949--1960},
refid = {Molenaar2018},
timestamp = {2018-12-07T18:05:16.000+0100},
title = {Wild-type and mutated IDH1/2 enzymes and therapy responses},
url = {https://doi.org/10.1038/s41388-017-0077-z},
volume = 37,
year = 2018
}