Haematologica

von Willebrand factor cleaving protease-ADAMTS 13

2026-09-04T08:19:38+00:00

The dilemma after chimeric antigen receptor T-cell therapy – to transplant or not?

2026-09-01T07:04:07+00:00

Conditioning for acute myeloid leukemia: looking beyond intensity

2026-09-01T07:04:08+00:00

Multiplex edited universal CAR T cells without the genomic cost

2026-09-01T07:04:09+00:00

Proteostasis meets signaling: UBE2G1 in hematopoietic stem cell aging

2026-09-01T07:04:10+00:00

Is it time to reduce the doxorubicin dosage in Hodgkin lymphoma therapy?

2026-09-01T07:04:12+00:00

The “Sweet” crosstalk between refractory leukemia cells and vascular niche

2026-09-01T07:04:12+00:00

Shaping the future of older patients with Philadelphia-negative lymphoblastic leukemia

2026-09-01T07:58:18+00:00

TP53 mutation analysis in myelodysplastic syndromes - long or short read sequencing?

2026-09-01T07:04:14+00:00

Older patients with lymphoma: navigating a landscape of clinical controversies and barriers to innovation

2026-09-01T07:04:15+00:00

Older patients with lymphoma represent a growing, heterogeneous population whose care is challenged by diverse outcomes, limited evidence, and one-dimensional age definitions. Historically, arbitrary age thresholds such as ≥60 or ≥80 years have guided treatment decisions, yet they fail to capture the biological and functional diversity of aging and can limit opportunities for cure and progress. Current practice relies on arbitrary dose reductions in old age, such as R-miniCHOP, despite limited data on optimal intensity and benefit–risk trade-offs. Likewise, novel agents and combination therapies frequently demonstrate discrepant efficacy and safety across age groups, but systematic attempts to optimize dose for older patients are rarely prioritized. When it comes to clinical trials, documenting benefit of new therapies is more challenging in older patients due to high background mortality, which complicates interpretation of overall and progression-free survival and may lead to underpowered trials. Moreover, prognostic models developed in younger populations have limited applicability in older patients, as they overlook the broader range of clinically relevant outcomes in older patients, including treatment-related mortality, functional decline, and quality of life. Pre-therapeutic geriatric assessments are prognostic, but their predictive capability remains to be demonstrated in prospective trials before use as treatment decision support tools. Addressing these challenges requires reframing of “old age” to a multidimensional construct, incorporating geriatric assessment, patients’ preferences, and biological age. More inclusive trial designs, dedicated dose-finding in older patients, and development of holistic, predictive models are critical to advance care. Without this, progress risks stalling for a growing group of our patients.

Preemptive hematopoietic stem cell transplantation in RUNX1 familial platelet disorder: a shared decision-making framework

2026-09-01T07:56:40+00:00

RUNX1 familial platelet disorder (RUNX1-FPD) is associated with a 35-50% lifetime risk of hematologic malignancy (HM). Like all germline HM predisposition syndromes, RUNX1-FPD can only be cured with allogeneic hematopoietic stem cell transplantation (HSCT). Current genetic screening techniques allow for early detection of germline predisposition and, consequently, the opportunity for HSCT before overt development of HM (i.e., preemptive HSCT). However, there is as yet no consensus on the use of preemptive HSCT for RUNX1-FPD. Described here is the case of an individual with RUNX1-FPD and a family history of HM who underwent preemptive HSCT. We introduce a shared decision-making framework designed to support individuals with RUNX1-FPD, their families, and their multidisciplinary clinical teams in evaluating whether and when to pursue preemptive HSCT versus continued surveillance. The framework reviews key medical factors that influence the decisions regarding timing of HSCT, including germline and somatic variants, clonal changes over time, familial history of HM, early morphologic or hematologic features, impacts on bleeding-related quality of life, and donor availability. The framework also summarizes the major risks and uncertainties potentially associated with preemptive HSCT while highlighting the associated ethical challenges. Together, the case and framework provide a structured, patient-centered approach for navigating the complex clinical decision of preemptive HSCT. Ongoing collaborative efforts to define cytogenetic and clonal changes preceding malignant transformation in RUNX1-FPD will refine the framework and bolster individualized treatment strategies aimed at preventing HM and improving the quality of life of individuals with RUNX1-FPD.

Hematopoietic cell transplantation after CD19-directed CAR T-cell therapy for remission consolidation or relapse treatment in pediatric acute lymphoblastic leukemia

2026-09-01T07:04:20+00:00

Relapse of B-cell acute lymphoblastic leukemia (B-ALL) after CD19-targeted chimeric antigen receptor T-cell therapy (CAR19) remains a substantial challenge. Allogeneic hematopoietic cell transplant (HCT) represents an approach for both post-CAR19 relapse prevention and relapse therapy. However, there is a paucity of detailed HCT safety and outcome data in this population. We conducted a retrospective review of 47 children and young adults with B-ALL who underwent first HCT for post-CAR19 remission consolidation (preemptive cohort, N=26) or relapse therapy (relapse cohort, N=21). With a median follow-up of 4.1 years, 3-year disease-free survival was 90% in the preemptive cohort and 64% in the relapse cohort. Overall survival, cumulative incidence of relapse, and non-relapse mortality at 3 years were 95%, 5%, and 5%, respectively, in the preemptive cohort and 67%, 20%, and 15%, repectively, in the relapse cohort. The cumulative incidence of grade 3-4 acute graft-versus-host disease (GvHD) was 14% in the preemptive cohort and 19% in the relapse cohort. Chronic GvHD developed in 24% and 14% of patients alive at 100 days in the preemptive and relapse cohorts, respectively. Veno-occlusive disease/sinusoidal obstruction syndrome was the most common non-GvHD severe organ toxicity, with a cumulative incidence of 10% in the preemptive cohort and 31% in the relapse cohort. In appropriate patients, HCT can be an effective strategy for attaining durable B-ALL remission when used preemptively after CAR19 or as part of post-CAR19 relapse salvage therapy.

Prognostic implications of myelodysplasia-related gene mutations in NPM1-mutated acute myeloid leukemia: a systematic review and meta-analysis

2026-09-01T07:04:25+00:00

NPM1-mutated (NPM1^mut) acute myeloid leukemia (AML) is generally classified as favorable-risk under the 2022 European LeukemiaNet (ELN-2022) guidelines, except in the presence of FLT3-internal tandem duplication or adverse-risk cytogenetics. However, the prognostic significance of co-occurring myelodysplasia-related gene (MRG) mutations remains unclear, with prior studies yielding inconsistent results. To clarify this issue, we conducted a systematic review and meta-analysis in accordance with PRISMA guidelines, searching PubMed, Embase, and MEDLINE through March 2025. MRG mutations were defined as pathogenic variants in ASXL1, BCOR, EZH2, SF3B1, SRSF2, STAG2, U2AF1, ZRSR2 and RUNX1, and the primary analysis incorporated studies regardless of RUNX1 inclusion. Data from ten cohorts across nine studies (1 of which included an independent validation cohort), encompassing a total of 4,363 patients, were analyzed. Of these, 655 patients (15.0%) harbored co-occurring MRG mutations. Among the patients with ELN-2022 intermediate risk (N=1,294), 108 (8.3%) had MRG mutations. The presence of MRG mutations was significantly associated with inferior overall survival (pooled hazard ratio [HR]=1.30; 95% confidence interval [CI]: 1.11-1.51; P<0.001; I²=39.2%), shorter event-free survival (HR=1.43; 95% CI: 1.11-1.85; P=0.006; I²=18.2%), and lower complete remission rates (risk ratio=0.94; 95% CI: 0.90-0.99; P=0.01; I²=0.0%). Subgroup analyses confirmed the adverse prognostic impact in patients receiving intensive therapy and those classified as ELN-2022 favorable risk. These findings suggest that MRG mutations confer an adverse prognostic effect in NPM1^mut AML and support the integration of MRG status into future risk stratification frameworks for NPM1^mut AML.

GvHD and GRFS in patients with acute myeloid leukemia undergoing allogeneic HCT with treosulfan- versus reduced-intensity busulfan-based conditioning: a subgroup analysis of a randomized phase 3 trial

2026-09-01T07:04:29+00:00

Acute myeloid leukemia (AML) is the most common indication for allogeneic hematopoietic cell transplantation (alloHCT), yet graft-versus-host disease (GvHD) remains a major post-transplant complication. Conditioning regimens, particularly reduced-intensity approaches, are critical in optimizing outcomes. This subgroup analysis of the phase III MC-FludT.14/L trial compared treosulfan-fludarabine with reduced-intensity busulfan-fludarabine in 352 AML patients (aged 31–70 years) undergoing alloHCT. The primary endpoint was 24-month event-free survival; secondary endpoints included overall survival, GvHD incidence, relapse/progression, and non-relapse mortality. Treosulfan compared to busulfan demonstrated superiority: 24-month event-free survival was 65% vs. 53% (P=0.01), and overall survival was 73% vs. 65%. Event-free survival benefits were consistent across AML risk categories and notably higher in patients with Hematopoietic Cell Transplantation Comorbidity Index score >2 (62% vs. 42%, P=0.02). Treosulfan also showed lower non-relapse mortality and relapse rates. GvHD outcomes favored treosulfan, with a significantly lower incidence of extensive chronic GvHD at 24 months (15.1% vs. 28.1%, P=0.01). GvHD-free and relapse-free survival was also improved (53% vs. 40%, P=0.02). The safety profile was more favorable with treosulfan. These findings support treosulfan-fludarabine as a more effective and safer conditioning regimen than busulfan-fludarabine for AML patients undergoing alloHCT, particularly those at higher risk.

Venetoclax and azacitidine for younger acute myeloid leukemia patients independent of fitness for intensive chemotherapy

2026-09-01T07:04:36+00:00

Venetoclax (ven) + azacitidine (aza) is the standard of care for newly-diagnosed acute myeloid leukemia (AML) patients who are not candidates for intensive chemotherapy (IC). Because prognostic factors for ven/aza and IC differ, an AML patient fit for IC may derive more benefit from ven/aza. We therefore designed a trial for younger, newly-diagnosed AML patients with non-favorable-risk disease to receive ven/aza regardless of “fitness” for IC (clinicaltrials gov. Identifier: NCT03573024). We aimed to understand toxicity and efficacy in this population, and retrospectively compared outcomes to matched IC patients. Newly-diagnosed non-favorable-risk patients ≤60 years old were enrolled and received ven, dose escalated to 600 mg/daily x28 days, with aza 75 mg/m2 x7 days on a 28-day cycle. Subjects were encouraged to move expeditiously to allogeneic stem cell transplant (ASCT) in first remission. Thirty-six subjects enrolled. Median age was 49 years (range, 22-59). Grade ≥3 neutropenia (42%), anemia (33%), thrombocytopenia (53%) and febrile neutropenia (36%) were common. The overall response rate (ORR) was 25 of 36 (69%) with 19 (53%) complete remissions; 68% of responders achieved MRD-negativity. Most subjects (53%) bridged to ASCT, and the majority of non-responders were successfully salvaged with IC. The median progression-free-survival and overall survival have not been reached (median follow-up 2.9 years). Compared to IC-matched controls, the ORR, ASCT rate and progression-free survival were significantly improved (69% vs. 44%; P=0.0495; 53% vs. 28%; P=0.0290; and not reached vs. 60.8 months; P=0.007). Hospital days, transfusions and infectious complications were significantly reduced for ven/aza subjects. Ven/aza is feasible for newly-diagnosed, younger, non-favorable-risk AML patients, and appears at least as effective as IC.

Phase I trial of autologous regulatory T cells for immune aplastic anemia

2026-09-01T07:04:41+00:00

Immune-mediated aplastic anemia (AA) is a bone marrow failure syndrome characterized by cytotoxic CD8-mediated autoimmune suppression of hematopoietic stem/progenitor cells resulting in varying degrees of peripheral blood cytopenias. Treatment with immunosuppressive therapy and hematopoietic stem cell transplantation are not applicable to all patients and effective responses occur in only a proportion of patients, highlighting the unmet need for alternative treatments. We have previously shown a reduction in the number and function of regulatory T cells (Treg) in AA patients and their functional restoration following in vitro expansion that laid the foundations for this phase I trial. Required numbers of Treg were collected from leukapheresis and expanded under Good Manufacturing Practice conditions from all six patients in the trial who were resistant/refractory to standard forms of treatment. The trial design included two doses of autologous Treg (5×106/ kg) administered 2 weeks apart. Mass cytometry, single-cell sequencing and cytokine profiling were performed on blood samples collected at various timepoints. Treg were successfully expanded to required doses from all six patients with no adverse or immune-related events in any of the patients. Hematologic responses were observed in three patients. In addition, we were able to track the persistence of the expanded Treg in vivo, correlate clinical efficacy with the accumulation of clusters of post-infusion Treg, and identify phenotypic markers in the infusion product that correlate with in vivo expansion. Treg from AA patients are expandable, safe for infusion, and may help to modulate the abnormal immune milieu associated with AA, with induction of clinical response. (Clinical-Trials.gov identifier: NCT05386264; EudraCT number: 2021- 000082-33).

Allo-defensive, multiplex base-edited, anti-CD38 CAR T cells for ‘off-the-shelf’ immunotherapy

2026-09-01T07:04:44+00:00

Chimeric antigen receptor (CAR) T-cell therapies are being widely investigated in both autologous and allogeneic settings, with gene editing providing new strategies to address barriers to mismatched cell therapies. Currently ‘universal’ donor-derived T-cell therapies require intensive lymphodepletion and are still prone to host-mediated rejection. CD38, a transmembrane glycoprotein involved in cell activation and bioenergetics, is a promising immunotherapy target for hematologic malignancies. Disruption of CD38 expression using base editing prevented fratricide between T cells expressing anti-CD38 CAR (CAR38). Additional base editing enabled generation of ‘universal’ donor CAR38-T cells, devoid of endogenous TCRαβ and human leukocyte antigen (HLA) molecules after disruption of T-Cell Receptor Beta Constant (TRBC), Beta-2 Microglobulin (B2M), and Regulatory Factor X5 (RFX5). Removal of cell surface HLA expression enabled evasion of anti-HLA antibodies in sera from sensitized donors and reduced allo-stimulation in mixed lymphocyte cultures, while TCRαβ disruption prevented allo-reactivity. In mixed lymphocyte cultures, CAR38 expression enabled potent ‘allo-defense’ activity against CD38+ allo-reactive cells. Multiplex base-edited CAR38-T cells exhibited antigen-specific antileukemic activity against human B, T, and myeloid malignancies and inhibited disease progression in humanized murine xenograft models. CAR38-T cells offer a potent ‘off-the-shelf’ strategy against CD38+ hematologic malignancies and long-lived plasma cells which can be associated with auto-antibody production.

Elevated levels of Ube2g1 in hematopoietic stem cells lead to segmental aging of the hematopoietic system

2026-09-01T07:04:48+00:00

Aged hematopoietic stem cells (HSC) show diminished capacity of self-renewal, skewed lineage output and compromised proteostasis. Ubiquitin proteasomal systems are critical for maintaining protein homeostasis. We show that the levels of Ube2g1, a E2 ubiquitin-conjugating enzyme likely involved in clonal selection of HSC, was elevated in aged murine and human HSC. We hypothesized that elevated levels of Ube2g1 causally contribute to hematopoietic system aging. Elevated levels of Ube2g1 in young murine HSC resulted in increased myeloid-to-lymphoid ratio and reduced naïve T cells, both known hallmarks of hematopoietic aging. Interestingly, the ubiquitination function of Ube2g1 did not primarily account for the observed phenotypes. Elevated levels of Ube2g1 affected global tyrosine phosphorylation, mediated through a Ube2g1-Shp2 axis, which correlated with impaired T-cell development and reduced HSC function. Our work identifies a novel connection between proteins involved in the regulation of ubiquitination and phosphorylation in HSC that affect phenotypes linked to aging of HSC.

The Znf711-Phf8 complex functions as a transcriptional rheostat essential for neutrophil development

2026-09-01T07:04:51+00:00

Neutrophil differentiation is governed by a precise transcriptional and epigenetic program. Here, we identify the zinc finger protein 711 (Znf711) and its partner, the histone demethylase PHD finger protein 8 (Phf8), as essential regulators of terminal granulopoiesis. Contrary to their established role as a transcriptional activator-co-activator pair, we found that the Znf711- Phf8 complex operates through a repressive mechanism. Znf711 promotes neutrophil maturation in a DNA-binding-independent manner by sequestering Phf8. Upon loss of Znf711, Phf8 is recruited by the growth factor independent 1 transcription repressor (Gfi1aa) to the promoter of the master regulator c/ebpα, where SUMOylated Phf8 acts as a corepressor to inhibit its transcription. Furthermore, we delineate a positive feedback loop wherein C/ebpα directly activates znf711 expression, ensuring a high level of c/ebpα at the onset of differentiation. Our findings define the Znf711-Phf8 complex as a critical transcriptional rheostat in neutrophil development.

Long-term cardiac morbidity in adolescent and young adult survivors of classical Hodgkin lymphoma: the British Columbia experience

2026-09-01T07:04:54+00:00

Adolescents and young adults (AYA) with classical Hodgkin lymphoma (cHL) have excellent survival outcomes. However, the late effects of treatment, including cardiovascular disease (CVD), can impact long-term disease-free morbidity and mortality. Using population-level administrative data, we evaluated rates of CVD in 2-year AYA survivors of cHL, aged 16-39 years, treated with ABVD or equivalent chemotherapy, with or without radiotherapy (RT). With a median follow up of 17 years (range 2.3-29 years), risk of CVD was 2.9-fold higher relative to controls, with a 5.2-fold risk of heart failure (HF) and 2.4-fold risk of ischemic heart disease (IHD). Risk of HF was associated with anthracycline-containing chemotherapy regimens alone or with combined modality therapy; whereas higher IHD risk was identified only in those treated with RT. At 20 years after the most recent cHL diagnosis or relapse, the cumulative incidence of HF was 4.3% in cases versus 0.8% in controls, and for IHD was 8.3% in cases versus 2.8% in controls. Treatment after 2005 using a PET scan guided approach reduced the overall use of RT (56.0% before 2005 vs. 14.9% 2005 and after), and was associated with a lower 15-year cumulative incidence of IHD (before 2005: 3.4% [95%CI: 1.8-5.1%]; 2005 and after: 0.7% [95%CI: 0-1.7%]) with the latter era comparable to controls; (1.6% [95%CI: 1.3-1.9%]). cHL survivors had increased 20-year cumulative mortality above that of age-matched controls (5.0% vs. 2.0%). These results can inform surveillance strategies, screening guidelines, and recommendations for risk factor modification for AYA cHL survivors.

Aberrant fucosylation of extracellular vesicles remodels the vascular microenvironment and promotes chemoresistance in myelodysplastic syndromes and acute myeloid leukemia

2026-09-01T07:04:57+00:00

Primary resistance to hypomethylating agents (HMA) remains a major obstacle in the treatment of elderly patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). An altered integrity of the vascular wall is suspected to contribute to this resistance, yet the underlying molecular mechanisms remain unclear. Here, we show that small extracellular vesicles (sEV) derived from leukemic cells resistant to decitabine (DAC-R), a commonly used HMA, promote vascular permeability by down-regulating tight junction proteins, including ZO-1, occludin and claudin5, in endothelial cell monolayers. This disruption of vascular integrity may facilitate vascular leakage and leukemic cell dissemination. Mechanistically, DAC-R cells exhibit increased expression of the fucosyltransferase FUT4, driven by the transcription factor TWIST1, leading to enhanced biosynthesis of non-sialylated Lewis x (LeX) structures. FUT4-mediated LeX modification stabilizes intercellular adhesion molecule 3 (ICAM3) on sEV, and the delivery of LeX-modified ICAM3 to endothelial cells suppresses NF-κB signaling, impairing endothelial barrier function. Functionally, vascular remodeling driven by fucosylated sEV promotes leukemic dissemination, suggesting that disruption of vascular homeostasis represents an additional layer of therapeutic resistance. These findings define a TWIST1–FUT4–LeX–ICAM3 axis and highlight glycosylation as a critical mediator of vascular microenvironment remodeling in MDS/AML.

Characterization of JNJ-80948543 a novel CD79bxCD20xCD3 trispecific antibody for B-cell non-Hodgkin lymphoma

2026-09-01T07:59:57+00:00

Despite advances in targeted therapies, in the majority of patients, relapsed/refractory B-cell non-Hodgkin lymphoma (R/R B-NHL) remains incurable. Thus, there is a critical need to expand the treatment options for R/R B-NHL to improve patient outcomes. In this study, we characterized JNJ-80948543, a novel trispecific T-cell engager (TCE), designed to target CD79b+ and/or CD20+ lymphoma cells and bind to CD3 T cells with low affinity. By engaging two tumor antigens, JNJ-80948543 may enhance tumor binding through avidity effects, potentially improving eradication of heterogeneous cell populations and reducing the risk of antigen escape. Preclinical data confirmed potent T-cell-mediated cytotoxicity against CD79b+ and/or CD20+ cells, with increased potency upon dual antigen engagement, consistent with an avidity effect. To mitigate the cytokine release syndrome and T-cell exhaustion commonly associated with TCE, JNJ-80948543 was designed with a low-affinity CD3 arm. In vitro, JNJ-80948543 achieved effective cytotoxicity with lower cytokine release compared to a matched high-affinity CD3 trispecific, JNJ-80948556. Despite reduced cytokine secretion by JNJ-80948543, both antibodies demonstrated comparable antitumor activity in a xenograft mouse model. Collectively, the selectivity, potent cytotoxicity, tumor growth inhibition, and favorable cytokine profile of JNJ-80948543 supports its clinical development. Phase 1 clinical trials are ongoing to evaluate JNJ-80948543 as a monotherapy (clinicaltrials.gov identifier NCT05424822) and in combination with a co-stimulatory bispecific antibody (clinicaltrials.gov identifier NCT06139406) in patients with R/R B-NHL.

REALiTEC: a multi-country observational retrospective study of teclistamab in patients with relapsed/refractory multiple myeloma outside of clinical trials

2026-09-01T07:05:09+00:00

Teclistamab is the first approved anti-B-cell maturation antigen (BCMA) bispecific antibody for patients with triple-class exposed relapsed/refractory multiple myeloma (RRMM), based on the results of the MajesTEC-1 clinical trial. Here, we first report the findings from REALiTEC, a retrospective observational study of patients who received teclistamab outside of clinical trials in Europe and Israel. The study included 113 patients from 23 sites in eight countries, with most (88.5%) accessing the medication through pre-approval access programs. The median age was 66 years, and patients had a median of 6 prior lines of therapy. Notably, 78.8% were triple-class refractory, 44.2% penta-class refractory, and 35.4% had previous anti-BCMA treatment. Overall response rate (ORR) was 60.2%, with 52.2% of patients achieving a very good partial response or better (≥VGPR). After a median follow-up of 20.7 months, median duration of response (DOR) was 20.3 months, median progression-free survival (PFS) was 9.7 months, and median overall survival (OS) was 26.3 months. Patients attaining ≥VGPR experienced longer DOR (median 26.1 months), with 12-month PFS and OS rates of 71.2% and 83.1%, respectively. Subgroup analyses demonstrated consistent outcomes across different patient groups, even in those with historically poorer outcomes. Most common adverse events were infections (all grades 70.8%), cytokine release syndrome (55.8%), neutropenia (35.4%), and anemia (25.7%), with no new safety signals identified. Infection rates decreased over time, and immunoglobulin replacement therapy was used in up to 60% of patients. REALiTEC corroborates the efficacy observed in the MajesTEC-1 study, supporting teclistamab as an effective treatment option in heavily pre-treated RRMM patients.

Platelet glycoprotein V autoantibodies and complement C3 are associated with thrombosis in systemic lupus erythematosus

2026-09-01T07:05:15+00:00

Systemic lupus erythematosus (SLE) is associated with an increased cardiovascular disease risk not fully explained by traditional factors. This retrospective study investigated the frequency and clinical relevance of platelet-specific glycoprotein (GP) autoantibodies and anti-phospholipid antibodies (aPL) in SLE. Serum from 89 patients with SLE (≥4 American College of Rheumatology 1982 criteria) was analyzed at higher (H) and lower (L) disease activity (median SLEDAI-2K: H=9.6 and L=2.1). Platelet GPIIb/IIIa-, GPV- and GPIb/IX-autoantibodies were detected using the indirect monoclonal antibody immobilization of platelet antigens assay, while immunoglobulin (Ig)M/IgG aPL, anti-β2 glycoprotein 1 (aβ2GP1), anti-cardiolipin (anti-CL), anti-phosphatidylserine/prothrombin complex (anti-PS/PT) and anti-annexin V (anti-AV) antibodies were measured by enzyme-linked immunosorbent assay. At high activity, 64% (57/89) of patients tested positive for at least one anti-GP antibody, compared to 42% (37/89) with low-disease activity. Anti-GPIIb/IIIa prevalence was stable (~30%), whereas anti-GPV and anti-GPIb/IX were more frequent during H (48% [43/89] vs. 24% [21/89] and 49% [44/89] vs. 27% [24/89], respectively). Anti-GPV levels correlated positively with SLEDAI-2K (r=0.34; P=0.001) and negatively with C3 and C4. Twenty-four patients developed unprovoked thromboembolic events during follow-up. In multivariate analysis, anti-GPV and C3 independently predicted thrombosis (hazard ratio [HR]=2.17; 95% confidence interval [CI]: 1.39-3.36; P=0.001; and HR=2.16; 95% CI: 1.32- 3.54; P=0.002). Platelet counts remained within the normal range irrespective of disease activity, antibody status or thrombotic events. In summary, platelet-specific anti-GP antibodies are prevalent in SLE patients. Anti-GPV, previously not studied in this context and complement C3, independently predicted thrombotic events.

Neutrophil extracellular traps, endothelial injury and use of abatacept for graft-versus-host disease prophylaxis

2026-09-01T07:05:16+00:00

CD19/CD22-targeted CAR T cells in autoimmune hemolytic anemia after allogeneic hematopoietic stem cell transplantation

2026-09-01T07:05:20+00:00

Sustained response off-treatment and thrombotic events in patients with immune thrombocytopenia treated with fostamatinib: a systematic review and meta-analysis

2026-09-01T07:05:23+00:00

Real-life management of 476 older adults with Philadelphia-negative acute lymphoblastic leukemia: a Campus ALL study

2026-09-01T07:05:25+00:00

HLA-DR expression at diagnosis is not predictive of relapse risk post allogeneic hematopoietic stem cell transplantation for pediatric acute myeloid leukemia: a report from the Children’s Oncology Group

2026-09-01T07:05:33+00:00

Extracellular vesicles from aged individuals trigger mitochondrial dysfunction in hematopoietic progenitor cells

2026-09-01T07:05:34+00:00

Pomalidomide, bortezomib and dexamethasone in multiple myeloma refractory to lenalidomide and anti- CD38 monoclonal antibodies: outcomes from a real-world experience

2026-09-01T07:05:38+00:00

The prognostic role of myeloid-related gene mutations in adult acute lymphoblastic leukemia

2026-09-01T07:05:43+00:00

Non-JAK-family gene fusions in cutaneous T-cell lymphoma highlights genetic diversity and potential therapeutic targets

2026-09-01T07:05:46+00:00

Phase I study of the safety and pharmacokinetics of CSL889 (hemopexin) in adults with sickle cell anemia

2026-09-01T07:05:48+00:00

Decoding the actionable potential of ribosome biogenesis in acute myeloid leukemia

2026-09-01T07:05:51+00:00

A systematic review of vaccine-induced immune thrombosis and thrombocytopenia triggered by non-adenoviral vector vaccination: ultra-rare or non-existent?

2026-09-01T08:01:13+00:00

Salvage high-dose chemotherapy and autologous stem cell transplant consolidation following relapse after CAR-T cell for large B-cell lymphoma

2026-09-01T07:05:53+00:00

B-cell precursor acute lymphoblastic leukemia with IGH::CEBP rearrangement: what have we learnt over the years?

2026-09-01T07:05:56+00:00

Long-read sequencing resolves TP53 allelic status in myeloid neoplasms

2026-09-01T07:05:57+00:00

Efficacy and safety of chimeric antigen receptor T-cell therapy for plasma cell leukemia

2026-09-01T07:05:58+00:00

SQSTM1::RARA fusion in acute promyelocytic leukemia: the first case report and literature review

2026-09-01T07:06:00+00:00

Myeloid blast phase of chronic myeloid leukemia with co-occurring t(11;12)(p15;q13)/NUP98::HOXC12: a novel NUP98 fusion partner

2026-09-01T07:06:01+00:00

Durable deep molecular response via CD19 chimeric antigen receptor T-cell therapy combined with a third-generation tyrosine kinase inhibitor in acute leukemia of ambiguous lineage with the Philadelphia chromosome: a potential strategy for transplant-ineligible patients

2026-09-01T08:04:36+00:00

Inherited HHV-6A reactivation linked to impaired immune reconstitution following hematopoietic stem cell transplantation

2026-09-01T07:06:05+00:00

Is it time to increase the liposomal doxorubicin dosage for frontline therapy in young adults and adults with classic Hodgkin lymphoma? Comment on: “Is it time to reduce the doxorubicin dosage in Hodgkin lymphoma therapy?”

2026-09-01T07:06:06+00:00

Response to Comment on: “Is it time to reduce the doxorubicin dosage in Hodgkin lymphoma therapy?”

2026-09-01T07:06:07+00:00