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. 2019 Feb 12;111(10):1033–1041. doi: 10.1093/jnci/djy230

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Published by Oxford University Press 2019. This work is written by US Government employees and is in the public domain in the US.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

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Figure 7. — Targeting NRF2 antioxidant pathway for IDH1-mutated cancers. IDH^WT cells exhibit normal reactive oxygen species (ROS) burden. NRF2 is recognized by KEAP1 and constitutively removed through proteasomal degradation. In IDH1^R132H cells, elevated ROS burden leads to NRF2 stabilization, nuclear translocation, and transcriptional activation of antioxidant genes. NRF2 downstream genes not only assist ROS homeostasis in IDH1-mutated cancer but also serve as potential resistance mechanism for chemotherapies.