Abstract
Activating KIT D816V mutations are frequently found in CBF AML, which predicts for an unfavorable outcome. Dasatinib is a potent inhibitor of wildtype and mutant-KIT isoforms – including D816V. We now provide proof of antileukemic efficacy in a patient with relapsing mutant-KIT D816V CBF AML. Importantly, this effect is mediated via overriding the differentiation blockage of the leukemia clone.In addition, we show that dasatinib is capable to induce pulmonary differentiation syndrome – and therefore needs close monitoring of patients under therapy.
Highlights
Activating KIT D816V mutations are frequently found in core binding factor (CBF) acute myeloid leukemia (AML) [1], predicting for an unfavorable outcome [2]
Activating KIT D816V mutations are frequently found in CBF AML, which predicts for an unfavorable outcome
We have previously shown that the BCR-ABL1 tyrosine kinase inhibitor dasatinib is a potent inhibitor of wildtype- and mutant-KIT, including the KIT D816V isoform, resulting in potent antiproliferative and proapoptotic efficacy [4]
Summary
Activating KIT D816V mutations are frequently found in core binding factor (CBF) AML [1], predicting for an unfavorable outcome [2]. We provide proof of antileukemic efficacy in a patient with relapsing mutant-KIT D816V CBF AML.
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