Harald Polzer, Hanna Janke, Schneider S, Wolfgang Hiddemann, Subklewe M and Karsten Spiekermann
FLT3 is a frequently mutated gene in acute myeloid leukemia that encodes a receptor tyrosine kinase. We report the case of a patient with FLT3-ITD positive secondary acute myeloid leukemia after treatment for breast cancer. Due to poor response to induction therapy and relapse before consolidation therapy we started a palliative treatment with the tyrosine kinase inhibitor sorafenib. After initial response clinical resistance occurred. Sequencing showed an additional FLT3-TKD mutation. Sunitinib effectively inhibited FLT3-ITD/TKD mutated cells in vitro and induced a reduction of blasts and prolonged survival in vivo. Individualized tyrosine kinase inhibitor therapy may prolong survival in selected patients with FLT3-ITD+ acute myeloid leukemia.
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