Figure 2.
Figure 2. Morphologic evidence of myeloid differentiation during enasidenib treatment. (A) Bone marrow (BM) blasts at screening (left). By cycle 3 day 1 (right), maturing forms including promyelocytes and myelocytes have largely replaced the immature myeloblasts, without initial marrow aplasia or hypoplasia at cycle 1 day 15 (middle). (B) Fluorescence in situ hybridization evidence of myeloid differentiation during enasidenib treatment. At screening, this patient with an IDH2-R140Q mutation had trisomy 8 in the majority of myeloblasts. By cycle 2 day 1, mature forms appeared with persistence of trisomy 8 in promyelocytes and mature granulocytes. In contrast, cells in the lymphoid compartment have a normal complement of chromosome 8.

Morphologic evidence of myeloid differentiation during enasidenib treatment. (A) Bone marrow (BM) blasts at screening (left). By cycle 3 day 1 (right), maturing forms including promyelocytes and myelocytes have largely replaced the immature myeloblasts, without initial marrow aplasia or hypoplasia at cycle 1 day 15 (middle). (B) Fluorescence in situ hybridization evidence of myeloid differentiation during enasidenib treatment. At screening, this patient with an IDH2-R140Q mutation had trisomy 8 in the majority of myeloblasts. By cycle 2 day 1, mature forms appeared with persistence of trisomy 8 in promyelocytes and mature granulocytes. In contrast, cells in the lymphoid compartment have a normal complement of chromosome 8.

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