Katharine E. Yen

TL;DR: It is shown that cancer-associated IDH1 mutations result in a new ability of the enzyme to catalyse the NADPH-dependent reduction of α-ketoglutarate to R(-)-2-hydroxyglutarate (2HG), and that the excess 2HG which accumulates in vivo contributes to the formation and malignant progression of gliomas.

TL;DR: Inducing differentiation of myeloblasts, not cytotoxicity, seems to drive the clinical efficacy of enasidenib, a first-in-class, oral, selective inhibitor of mutant-IDH2 enzymes.

TL;DR: The recent discovery of mutations in metabolic enzymes has rekindled interest in harnessing the altered metabolism of cancer cells for cancer therapy, and isocitrate dehydrogenase 1 (IDH1), which is mutated in multiple human cancers, is examined.

TL;DR: In patients with advanced IDH1‐mutated relapsed or refractory AML, ivosidenib at a dose of 500 mg daily was associated with a low frequency of grade 3 or higher treatment‐related adverse events and with transfusion independence, durable remissions, and molecular remissions in some patients with complete remission.

TL;DR: Evidence is provided that inhibitors targeting mutant IDH2/R140Q could have potential applications as a differentiation therapy for cancer, and a small molecule, AGI-6780, that potently and selectively inhibits the tumor-associated mutant IDh2/ R140Q is developed.