Elodie Pronier, Ross L. Levine Cancer Cell

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IDH1/2 Mutations and BCL-2 Dependence: An Unexpected Chink in AML’s Armour Elodie Pronier, Ross L. Levine Cancer Cell Volume 27, Issue 3, Pages 323-325 (March 2015) DOI: 10.1016/j.ccell.2015.02.013 Copyright © 2015 Elsevier Inc. Terms and Conditions

Figure 1 Synthetic Lethal Mechanism between IDH1/2 Mutations and BCL-2: Definition of a New Therapeutic Target (A) (R)-2HG, generated by IDH1/2 mutants, inhibits cytochrome c release by complex IV (COX), which activates BAX/BAK signaling that is blocked by BCL-2 activity, allowing cell survival. (B) ABT-199 treatment of IDH1/2-mutated cells permits full activation and oligomerization of BAX/BAK proteins, resulting in mitochondrial outer membrane permeabilization (MOMP)-induced apoptosis. Cancer Cell 2015 27, 323-325DOI: (10.1016/j.ccell.2015.02.013) Copyright © 2015 Elsevier Inc. Terms and Conditions