Dasatinib overrides the differentiation blockage in a patient with mutant-KIT D816V positive CBFβ-MYH11 leukemia
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Kerstin M. Kampa-Schittenhelm1, Wichard Vogel1, Irina Bonzheim2, Falko Fend2, Marius Horger3, Lothar Kanz1, Martin Soekler1 and Marcus M. Schittenhelm1
1Department of Oncology, Hematology, Rheumatology, Clinical Immunology and Pulmonology, University Hospital Tübingen, Tübingen, Germany
2Institute of Pathology and Neuropathology, Reference Center for Hematopathology, University Hospital Tübingen, Tübingen, Germany
3Department of Diagnostic and Interventional Radiology, University Hospital Tübingen, Tübingen, Germany
Marcus M. Schittenhelm, email: email@example.com
Keywords: CBF AML; KIT; tyrosine kinase inhibition; differentiation
Received: September 18, 2017 Accepted: January 15, 2018 Published: January 31, 2018
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.
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