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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.
This article elucidates how the TCA cycle enzyme IDH3 critically regulates metabolic fitness in AML stem cells, influencing venetoclax resistance and offering a novel target to improve therapeutic outcomes.
This review synthesizes cutting-edge findings on how genetic and nongenetic RAS-pathway activation mediates resistance to combined FLT3 and BCL2 inhibition in acute myeloid leukemia, highlighting implications for treatment strategies and bi
A large registry analysis supports post-transplant cyclophosphamide (PTCy) as an effective alternative to anti-thymocyte globulin (ATG) for preventing graft-versus-host disease (GVHD) in reduced-intensity conditioning matched donor peripher
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
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.
Oral decitabine/cedazuridine plus venetoclax provides an effective, fully oral frontline therapy for older or unfit patients with AML, showing encouraging response rates and manageable safety with long-term follow-up, highlighting particula
Fludarabine, cyclophosphamide, and low-dose TBI combined with post-transplant cyclophosphamide provide a safe and effective single platform for haploidentical and unrelated donor allo-SCT in older AML/MDS patients, showing favorable surviva
BRAF mutations occur in about 1% of AML and are usually non-V600 variants enriched in myelodysplasia-related disease. This cohort study found poor survival and suggested that current therapies, including venetoclax-based regimens, remain in
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.
A phase 1 trial suggests briquilimab can be safely added to nonmyeloablative conditioning before allogeneic transplant in older adults with high-risk AML or MDS, with biologic evidence of hematopoietic stem/progenitor cell depletion and enc
MD-265, a PROTAC MDM2 degrader, showed strong anti-leukemia activity in primary AML cells and mouse PDX models, outperformed a conventional MDM2 inhibitor, and spared normal stem cells relatively well.
Post-cycle 2 CBFB::MYH11 MRD best predicted outcomes in favorable-risk AML. Patients with levels ≥1% had higher relapse risk, and those receiving allo-HCT in CR1 had better 3-year disease-free survival than chemotherapy consolidation.
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
VCAR33, a donor-derived anti-CD33 CAR T-cell therapy, demonstrated acceptable safety and preliminary efficacy in relapsed/refractory AML/MDS after allogeneic HCT, with 20% overall response rate and manageable toxicities.
A study of 48 patients with R/R AML treated with revumenib revealed that 52% experienced dynamic immunophenotypic changes. Achieving MRD-negative morphologic remission significantly improved overall survival, highlighting the necessity for
Recent research identifies BMPR1B and TAZ/TEAD as critical mechanotransduction drivers in relapsed AML. By targeting these pathways, clinicians may overcome the protective effects of bone marrow stiffening and intramedullary pressure, offer
Researchers identify a novel NSUN2-FOSB-BCL2L1 regulatory axis in AML that drives leukemia stem cell self-renewal through m5C RNA methylation. This pathway offers a potential therapeutic target that spares normal hematopoiesis, suggesting a
This review explores oncofetal chondroitin sulfate (ofCS) as a revolutionary AML target. Unlike traditional antigens, ofCS is absent in normal bone marrow, allowing antibody-drug conjugates to eliminate leukemia cells with minimal hematotox
