AI Article Synopsis
- A novel Y842D mutation in the FLT3 gene has been identified in a pregnant patient with acute myeloid leukaemia (AML), which has been linked to resistance against the drug sorafenib.
- The patient initially did not respond to standard chemotherapy but later achieved remission after treatment with midostaurin, a targeted therapy for mutant-FLT3, combined with conventional drugs.
- During the midostaurin treatment, the patient experienced differentiation syndrome, which was successfully managed with methylprednisolone, indicating that the Y842D mutation might be sensitive to midostaurin therapy in AML cases.
Article Abstract
A Y842D mutation within the activation loop of fms-like tyrosine kinase 3 (FLT3) has been shown to confer strong resistance to sorafenib . Whether this type of mutation exerts clinically significant effects in patients with acute myeloid leukaemia (AML) remains unclear. Here, a novel Y842D activating mutation within the kinase domain of FLT3, in a pregnant patient with de novo hyperleucocyte acute myeloid leukaemia, is described. Following induction failure with standard dose idarubicin and cytarabine (IA), the patient received 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 that was characteristic of differentiation syndrome, which disappeared following treatment with methylprednisolone. The present case revealed that Y842D, an uncommon activating mutation in the activation loop of FLT3, may be a midostaurin-sensitive mutation type in patients with acute myeloid leukaemia.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9251825 | PMC |
| http://dx.doi.org/10.1177/03000605221097774 | DOI Listing |
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