A Novel FLT3 Y842D Mutation Carriers a Potentially Highly Sensitivity to Midostaurin? Case Report and Literature Review

Abstract

Background: Y842D mutation in the activation loop of FLT3 caused a strong resistance to Sorafenib in vitro, whether this kind of mutation would exert clinical significance on acute myeloid leukemia (AML) patients remain to be clarified.Case presentation: Here, we described a novel type of activating mutation (Y842D) within the kinase domain of FLT3 in a pregnancy with de novo acute myeloid leukemia. Following induction failure with standard dose of idarubicin and cytarabine (IA), the patient received a re-induction combined with midostaurin, a promising agent targeting mutant-FLT3, and IA regimen. Fortunately, morphological remission was achieved. During the period of midostaurin treatment, the patient exhibited a symptom which was quite similar to the differentiation syndrome which disappeared following the treatment with methylprednisolone. Conclusions: Clinically, we showed for the first time that Y842D, a novel activating mutation in the activation loop of FLT3, tend to be a sensitive mutation form to midostaurin in acute myeloid leukemia patients.

Application of 'preventive treatment of disease' theory in hyperthyroidism

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