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Targeting the mitochondrial complex I subunit NDUFS2 enhances sensitivity to FLT3 inhibitors and overcomes drug resistance in acute myeloid leukemia with FLT3-ITD mutations, suggesting a promising therapeutic strategy.
The INTERVENE trial reveals that adding midostaurin to low-dose cytarabine and venetoclax is tolerable and improves FLT3-ITD clearance and survival in older AML patients with FLT3-ITD, addressing resistance in this high-risk subgroup.
The ELN‑DAVID 2026 technical note establishes standards for NGS-based detection of FLT3‑ITD measurable residual disease (MRD) in AML, with lab validation, reporting, timing, and clinical-use recommendations to make FLT3‑ITD MRD testing acti
Low-level FLT3-ITD microclones, detected via NGS in young adults with AML, independently increase relapse risk comparable to macroclones, challenging current risk stratification and underscoring the need to integrate advanced genetic testin
FLT3-ITD mutations in AML promote immune evasion through a novel PKCι–STAT1 signaling axis that induces CD276-mediated CD8+ T-cell exhaustion, offering a promising target for combined FLT3 and CD276-directed therapies.
Preclinical data suggest fingolimod and mocravimod can resensitize NRAS-mutated FLT3-ITD AML to FLT3 inhibitors by suppressing ERK-SPHK1-AKT signaling, including activity in patient blasts and an orthotopic mouse model.
Adult AML with NUP98 rearrangements is a high-risk subtype marked by frequent FLT3-ITD and WT1 mutations, poor survival, and potential benefit from FLT3 inhibitors and stem cell transplant.
A large EBMT study shows allo-HSCT provides favorable 2-year survival (65.7%) in high-risk t(6;9) AML, with superior outcomes in CR1 and pediatric/AYA patients. FLT3-ITD positivity triples relapse risk but doesn’t impact overall survi
Posttransplant gilteritinib greatly benefits FLT3-ITD AML patients with NPM1 comutations, while myeloablative conditioning offers limited advantages over reduced-intensity conditioning in eradicating measurable residual disease.
