Erica Tobin

TL;DR: It is shown that the targeted inhibitor AG-221 suppresses the mutant IDH2 enzyme in multiple preclinical models and induces differentiation of malignant blasts, supporting its clinical development.

TL;DR: AG-120 (ivosidenib), an inhibitor of the IDH1 mutant enzyme that exhibits profound 2-HG lowering in tumor models and the ability to effect differentiation of primary patient AML samples ex vivo is reported.

TL;DR: Clinical data is provided showing that mutant IDH2 expression is restricted to malignant T cells and that 2HG may be a useful biomarker in AITL and conditional knock-in mouse models show that in the lymphoid system, mutations in IDH 2 at R172 produce high levels of 1HG compared with mutations at the other two sites and that lymphoid development is impaired in these animals.

TL;DR: It is demonstrated that combining IVO + AZA in the TF1-IDH1R132H AML cell line enhanced cell differentiation, as measured by increases in hemoglobinization and expression of differentiation markers, and potentiated cell death, compared with either agent alone.

TL;DR: It is shown that Idh1 mutations can contribute to the development of T-cell malignancies, including T-ALL, using a conditional knock-in mouse model, and this data suggest that mutant IDH1 contributes to malignancy in the T- cell lineage and may alter the metabolic profile of malignant T cells.