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Dysfunction in SLF2 and SMC5 causes premature hematopoietic stem cell aging, bone marrow failure, and early-onset myelodysplastic syndrome in Atelis Syndrome, defining a novel inherited bone marrow failure disorder.
RAAS inhibitors, used for kidney protection in sickle cell disease, may significantly exacerbate anemia by impairing erythropoiesis, warranting close hemoglobin monitoring in this vulnerable population.
This study evaluates non-invasive biomarkers to differentiate essential thrombocythemia, premyelofibrosis, and overt myelofibrosis, revealing distinct inflammatory and immune profiles and supporting a disease continuum model.
Biallelic loss-of-function mutations in BPNT1 are identified as a new genetic cause of vitamin B12-dependent megaloblastic anemia, linked to disrupted ribosome biogenesis and impaired ileal vitamin B12 absorption in mouse models.
This study evaluates the incidence, severity, and predictors of extracranial bleeding in atrial fibrillation patients on oral anticoagulants, highlighting its substantial burden beyond major bleeds and informing bleeding risk management.
This multicenter study evaluates autologous stem cell transplantation (ASCT) in POEMS syndrome, showing significant hematologic response, durable survival, and manageable toxicity, highlighting ASCT’s pivotal role in treatment.
Anti-PD-1 therapy has transformed classical Hodgkin lymphoma management, demonstrating safety, feasibility, and durable efficacy across treatment settings—from relapsed/refractory disease to frontline therapy.
BIA-ALCL is a heterogeneous T cell lymphoma marked by immunosuppressive tumor microenvironments that promote tumor survival and proliferation, revealing potential targets for advanced disease therapy.
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
This retrospective EBMT study identifies secondary autoimmune and inflammatory diseases as rare but significant complications following allo-HSCT, highlighting their incidence, risk factors, and impact on patient survival, calling for impro
This study reveals that certain high-risk cytogenetic abnormalities continue to influence progression-free survival in multiple myeloma patients even after achieving deep MRD negativity post-ASCT, highlighting the need for tailored post-tra
A prospective study finds that baseline EASIX and day 14 sC5b-9 are independently associated with TA-TMA after allo-HCT, with combined stratification identifying high-risk adults.
Five-year results from the OPTIC trial show that starting ponatinib at 45 mg then reducing to 15 mg upon response provides the best long-term efficacy and manageable safety in resistant CP-CML, particularly for T315I patients.
A study of 2,577 haploidentical transplants shows that extended HLA haplotypes, including a class III SNP, significantly influence mortality and relapse, potentially improving donor selection.
A phase 1 trial of ultralow-dose IL-10–expressing CD19 CAR T cells in 13 patients with R/R DLBCL reported a 92.3% objective response rate with manageable safety.
This review synthesizes evidence on the role of RNA-binding protein G3BP2 in conferring venetoclax resistance in AML through stabilizing ELF1 mRNA and upregulating MCL1 transcription, highlighting novel therapeutic avenues combining G3BP2 i
In AML patients receiving frontline azacitidine and venetoclax, achieving measurable residual disease negativity strongly predicts longer survival and lower relapse rates, overriding baseline risk factors, as shown in the French VENAURA reg
The GRAALL-2014/B-QUEST study demonstrates that integrating blinatumomab into consolidation and maintenance therapy significantly improves outcomes for adults with high-risk Philadelphia chromosome-negative B-cell acute lymphoblastic leukem
This review highlights how EIF4A3-dependent nonsense-mediated mRNA decay selectively regulates the oncogenic AML1-ETO9a isoform in t(8;21) AML, influencing leukemic cell proliferation, chemosensitivity, and patient survival through an isofo
MDM4 haploinsufficiency activates p53, causing diverse bone marrow failure phenotypes and hypocellular MDS, highlighting the pivotal MDM4-p53 axis in hematopoietic regulation and potential targets for intervention.
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