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Center point:
Center point:When drug resistance or disease progression occurs, about 50% of patients treated with Mistalin have FLT3-ITD negative
When drug resistance or disease progression occurs, about 50% of patients treated with Mistalin have FLT3-ITD negativeThe persistent FLT3-ITD positive may be caused by the selection of resistant FLT3 clones, the mechanism is to bypass FLT3 inhibition or insufficient drug activity
The persistent FLT3-ITD positive may be caused by the selection of resistant FLT3 clones, the mechanism is to bypass FLT3 inhibition or insufficient drug activityIn the international randomized phase 3 RATIFY trial (a randomized trial of FLT3 in AML patients aged 60 years and under), the multikinase inhibitor Midostaurin significantly improved FLT3 mutant acute myeloid leukemia between 18-50 years of age (AML) The overall survival and event-free survival of the patient
Only 59% of patients in the Mistalin group achieved a protocol-specific complete remission (CR), and almost half of the patients who achieved CR had relapses
In order to explore the potential mechanism of resistance in patients with FLT3 mutant AML, Schmalbrock et al.
FLT3-ITD routine Genescan detection and whole-exome sequencing were performed on paired samples collected from 54 patients at the time of diagnosis and at the time of relapse/refractory treatment
The FLT3-ITD mutation in the test patient at diagnosis or recurrence/progression
The FLT3-ITD mutation in the test patient at diagnosis or recurrence/progressionWhen the disease acquires drug resistance or progresses, almost half of the patients (46%) become FLT3-ITD negative , but at the same time acquire a signaling pathway (such as MAPK), thereby gaining a new proliferative advantage
When the disease acquires resistance or progresses, almost half of the patients (46%) become FLT3-ITD negative
Gene mutation changes in relapsed patients at diagnosis and relapse
Gene mutation changes in relapsed patients at diagnosis and relapseIn 32% of cases, no changes in FLT3-ITD mutations were observed, indicating that the resistance mechanism bypassed FLT3 inhibition or due to insufficient drug levels, the inhibitory activity of Mistaline was lost
In 32% of cases, no changes in FLT3-ITD mutations were observed, indicating that the resistance mechanism bypassed FLT3 inhibition or that the inhibitory activity of Mistaline was lost due to insufficient drug levels
In conclusion, this study provides new insights into the clonal evolution and resistance mechanisms of AML patients with FLT3-ITD mutations under the treatment of Mistalin combined with intensive chemotherapy
Original source:
Original source:Schmalbrock Laura K,Dolnik Anna,Cocciardi Sibylle et al.
Clonal evolution of acute myeloid leukemia with FLT3 -ITD mutation under treatment with midostaurin
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