Answers are grounded in this paper and cite their sources.
The FMS-like tyrosine kinase 3 (FLT3) domain is the most mutated gene in acute myeloid leukemia (AML), with FLT3 internal tandem duplication (ITD) mutations conferring adverse outcomes [1,2].Maintenance therapy after hematopoietic stem cell transplant (HSCT) may be essential, as FLT3 AML patients experience high rates of post-HSCT relapse and mortality [3].Terao et al. found that relapsed/refractory (R/R) FLT3 AML patients who received post-HSCT maintenance gilteritinib had improved overall survival (OS) (1-year OS, 100% vs. 45.5%,p = 0.0075) and cumulative incidence of relapse (CIR, 1-year CIR 0% vs. 68.8%,p = 0.0028) [4].However, the phase 3 MORPHO trial failed to reach the primary outcome of improved relapse-free survival (RFS) with post-HSCT maintenance gilteritinib compared to placebo in FLT3-ITD AML patients except in measurable residual disease (MRD) positive patients [5].As prospective data on FLT3 inhibitor maintenance therapy are evolving, there is a need to investigate real-life data and outcomes to guide clinical decisions.
No takes yet. Share an insight, caveat, or question.
Ashouri et al. (2024) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: