Haematologica

Humoral influence on cytotoxicity in myeloid leukemia therapies

2026-08-01T20:04:32+00:00

RBM15 and ZMYND8 shape acute myeloid leukemia response to BCL2 inhibitors

2026-08-01T10:01:21+00:00

Circulating T follicular helper cells as emerging biomarkers in pediatric Evans syndrome

2026-08-01T10:01:22+00:00

Relapse as a return, not a reinvention — genomic stability and pre-existing resistance in mantle cell lymphoma

2026-08-01T10:01:23+00:00

Myeloid neoplasms after follicular helper T-cell lymphomas: a real, but limited risk

2026-08-01T10:01:25+00:00

Unmasking the invisible: CAR T-cell therapy for intravascular large B-cell lymphoma

2026-08-01T10:01:26+00:00

Post-CAR-T lymphocytosis in multiple myeloma: too much of a good thing?

2026-08-01T10:01:27+00:00

To B or not to B, that is the question: the role of bleomycin in early stage Hodgkin lymphoma

2026-08-01T10:01:28+00:00

Translocation t(11;14) and BCL2-inhibition in multiple myeloma

2026-08-01T10:01:29+00:00

Multiple myeloma is an increasingly treatable disease with improved survival, although characterized by multiple subclones that drive heterogeneity and variable clinical outcomes between patients. A biomarker-driven approach can help to tailor treatment and improve patient outcomes. Translocation t(11;14), a primary cytogenetic abnormality present in 15-20% of myeloma patients at diagnosis, is currently the most prominent targetable lesion in myeloma. In the era of induction with proteasome inhibitors and/or immunomodulatory drugs, t(11;14) has been associated with poorer outcomes compared to other standard-risk subgroups, with shorter progression-free and overall survival. The presence of t(11;14) in myeloma cells confers increased dependence on the pro-survival BCL2 protein, thus driving its ability to evade apoptosis, and is the main biomarker predicting response to BCL2-inhibitors. This review examines the pathogenesis and prognostic significance of t(11;14) in myeloma and the impact of concurrent high-risk cytogenetics, the mechanism of action of BCL2-inhibitors, cumulative evidence supporting their use, and proposed mechanisms of resistance. The review also presents potential future directions regarding BCL2-inhibitor-based regimens and how best to position these drugs to optimize patient outcomes.

Preserving thrombosis and life years in polycythemia vera: start by reading the biology of the disease

2026-08-01T10:01:31+00:00

The Swedish nationwide study by Leontyeva et al., published in Haematologica in September 2025, revealed that patients with myeloproliferative neoplasms (MPN) continue to lose life years compared with the general population, with polycythemia vera (PV) showing a 1.8-year loss in restricted mean survival at 15 years. Despite being classified as “low risk,” these younger patients lose more life years than age-matched peers. They face decades of exposure to clonal proliferation, inflammation, and thromboinflammation, which contribute to vascular injury, myelofibrosis, and secondary cancers. Evidence suggests that early, biology-guided therapy may modify this trajectory. Interferon (particularly ropeginterferon alfa-2b) and ruxolitinib reduce JAK2^V617F allele burden, systemic inflammation (as reflected by the neutrophil-to-lymphocyte ratio [NLR]), and thrombosis rates, demonstrating long-term disease-modifying potential. The challenge lies in identifying which younger patients should receive cytoreductive therapy, as these treatments, while effective, may be poorly tolerated or burdensome over decades. Biological markers such as persistent leukocytosis, elevated NLR, rising JAK2^V617F variant allele frequency, or high phlebotomy burden can guide treatment decisions more precisely than age alone. Tailoring therapy in younger PV patients according to disease biology and individual tolerance may prevent irreversible complications, improve quality of life, and ultimately reduce the number of life years lost.

Successful re-exposure to high-dose methotrexate after severely delayed methotrexate elimination and renal toxicity in children with acute lymphoblastic leukemia

2026-08-01T10:01:33+00:00

High-dose methotrexate (HDMTX) is a cornerstone of contemporary treatment protocols for both pediatric and adult acute lymphoblastic leukemia (ALL); however, up to 4% of children and 15% of adults develop renal toxicity with severely delayed MTX elimination (DME). Evidence-based guidance on re-exposure after DME is lacking, and omission of further HDMTX may compromise anti-leukemic efficacy and potentially increase the risk of relapse. This study, conducted within the Ponte di Legno International Toxicity Working Group, aimed to evaluate the safety of HDMTX re-challenge in pediatric patients after DME. National investigators from 12 countries provided case-level data on initial DME events and subsequent HDMTX re-exposures via structured questionnaires. Data from 189 patients treated for ALL who experienced DME were analyzed, of whom 143 were subsequently re-exposed to HDMTX. Clinical toxicities after the initial DME included gastrointestinal complications (vomiting, diarrhea, mucositis), infections, and neurological events (encephalopathy, seizures, MTX stroke-like syndrome). Laboratory toxicities comprised cytopenias and hepatic abnormalities. Two patients transiently required dialysis. DME led to chemotherapy modifications in 73% of the patients. After re-exposure, toxicities were similar in spectrum, self-limited, and non-fatal. Twenty children (14%) developed recurrent DME, including three with two additional episodes. Recurrent DME could neither be predicted by clinical, pharmacokinetic, or demographic variables, nor by uniform MTX dose reduction during re-exposure. In conclusion, re-exposure to HDMTX following DME is feasible and generally well tolerated, although the risk of recurrence is increased. Re-challenge should be considered once renal function has normalized, with careful monitoring and individualized dose adjustment.

m6A and NuRD complexes regulate monocytic differentiation and resistance to BCL2/BCL2L1 inhibitors in acute myeloid leukemia

2026-08-01T10:01:37+00:00

Frontline use of the BCL2 inhibitor, venetoclax, for acute myeloid leukemia (AML) has resulted in broad improvements in patients’ outcomes. A major remaining challenge is the development of venetoclax resistance, frequently driven by compensatory transcriptional programs that promote cell survival and differentiation. These changes reduce dependence on BCL2 in favor of alternative anti-apoptotic BCL2 family members such as MCL1 or BCL2L1 (BCL-XL). Using CRISPR-based genome-wide perturbation screens, we investigated the genetic dependencies of venetoclax and the BCL2/BCL2L1 dual inhibitor AZD4320. We identified the N6-methyladenosine (m6A) writer RBM15, and the nucleosome remodeling and deacetylase (NuRD) complex interactor ZMYND8 as novel mediators of resistance to both venetoclax and AZD4320. Loss of RBM15 or ZMYND8 induced drug resistance, concurrent with alterations in BCL2 family expression and monocytic differentiation. Accordingly, in AML patients’ samples we found reduced expression of the respective m6A or NuRD complexes was significantly associated with monocytic differentiation and ex vivo resistance to the same drugs. These findings provide critical insights into previously undescribed mechanisms of BCL2 family inhibitor resistance in AML.

ICANS mitigation in high-risk elderly patients treated with CD28 co-stimulatory anti-CD19 CAR-T cells using a standardization protocol: a pilot study

2026-08-01T10:01:40+00:00

Chimeric antigen receptor T-cell therapy (CAR-T) has transformed the treatment of relapsed/refractory large B-cell lymphoma (LBCL), with CD28-based products yielding rapid responses but higher rates of immune effector cell-associated neurotoxicity syndrome (ICANS). With axicabtagene-ciloleucel and brexucabtagene-autoleucel, overall and severe ICANS reach 78% and 35%, respectively. Older adults are vulnerable, yet mitigation strategies are still lacking. To address this critical gap, we aimed to develop and implement a standardized ICANS mitigation protocol for older adults receiving CD28-based anti- CD19 CAR-T. We conducted a single-arm prospective pilot study in patients ≥75 or ≥65 years with additional risk factor receiving CD28-based CAR-T. The protocol included levetiracetam and thiamine prophylaxis, early grade-based corticosteroids and anakinra for grade ≥3 and refractory ICANS, which was defined as no improvement within 24 hours. Endpoints were ICANS duration, refractoriness, response, and toxicity. Forty-five patients met eligibility criteria. Median age was 75 years (range: 65-86 years); 78% had Eastern Cooperative Oncology Group (ECOG) ≥2 and 42% had neurologic comorbidity. Grade ≥3 and refractory ICANS developed in 67% overall, with grade ≥3 in 31%, and refractory ICANS in 20%. Median ICANS duration was four days, which was shorter than previous cohorts. Disease and patients’ characteristics did not predict ICANS metrics, excluding lactate dehydrogenase which showed a trend for severe ICANS (P=0.07). modified Endothelial Activation and Stress Index (mEASIX) and ICANS-Prognostic Scoring System (PSS) scores were not predictive and expansion was not compromised. Cumulative steroids associated with infections (P=0.002) and non-relapse mortality (P<0.0001). Sixmonth progression-free survival and overall survival were 46% and 59%, respectively. In this high-risk cohort, the ICANS mitigation protocol using anakinra in a graded approach (vs. prophylaxis or salvage therapy) and a pragmatic definition of refractory disease was associated with shorter ICANS duration, despite severe event rates. Steroid-related toxicity remains a concern, and future efforts should focus on steroid-sparing mitigation to optimize outcomes in older adults undergoing CAR-T.

Real-world outcomes in refractory chronic graft-versus-host disease: the Italian multicenter experience with belumosudil

2026-08-01T10:01:44+00:00

Chronic graft-versus-host disease (cGvHD) remains a major late complication of allogeneic hemato-poietic stem cell transplantation, leading to impaired quality of life and late non-relapse mortality. Belumosudil, an oral ROCK2 inhibitor with immunomodulatory and antifibrotic properties, represents a novel treatment for steroid-refractory or steroid-dependent cGvHD. We conducted a retrospective, multicenter study of 80 patients treated with belumosudil across 29 Italian transplant centers through a compassionate use program. Patients were heavily pretreated (74% with ≥3 prior lines, 84% previously exposed to ruxolitinib), with severe disease in 86% and a median of three organs involved. The best overall response rate was 62.5%, while overall response rates were 52.6%, 57.6%, and 55.0% at three, six, and 12 months, respectively. Median time to response was three months, and the 12-month duration of response was 83.4%. Failure-free survival at 12 months was 67.5%. Responses were observed in all involved organs. Patient-reported outcomes assessed through the National Institutes of Health Severity Index Score (0-10 scale) showed meaningful improvements (≥-2 points) in 33%, 36%, and 29% of patients at three, six, and 12 months, respectively. Treatment was well tolerated. These real-world findings confirm the effectiveness of belumosudil in patients with cGvHD refractory to multiple lines of immunosuppressive therapy.

Fibrin-bound thrombin determines clot structure and blood thrombogenicity in normofibrinogenemia and dysfibrinogenemia

2026-08-01T10:01:49+00:00

In thrombosis and hemostasis, coagulation and platelet activation pathways culminate to form solid fibrin clots, which can become vaso-occlusive or prevent excessive bleeding. We report a novel mechanism describing how developing fibrin clots prolong and modulate the reactivity of thrombin, an enzyme propagating platelet and coagulation activation and forming fibrin from fibrinogen. Using immunological and genetic approaches, we delineate how thrombin bound to the Aa and Bb chains of fibrin E-domains regulates lateral fibrin fiber extension. Our data reveal that fibrin-bound thrombin remains active and is temporarily protected against inactivation by antithrombin-III. Immunological displacement of thrombin from fibrin profoundly lowered its capacity, whereas a peptide mimicking the Aa-chain binding-site increased its reactivity. In a cohort of patients with congenital dysfibrinogenemia, carrying FGA, FGB or FGG mutations associated with bleeding or thrombosis phenotypes, we noticed a high thrombin capacity and suppressed thrombin-antithrombin-III complex formation, pointing to a prolonged active thrombin lifetime, likely due to abnormal formation of thrombin-containing fibrin. In conclusion, the combination of impaired clotting and increased thrombogenicity may explain the paradoxical bleeding and thrombotic complications observed in such patients. Development of fibrin-directed agents may offer new therapeutic opportunities to normalize hemostasis or prevent thrombosis.

Extracellular microvesicles from patients with antiphospholipid syndrome carry antigenic targets and promote endothelial cell activation in vitro

2026-08-01T10:01:55+00:00

Antiphospholipid syndrome (APS) is characterized by thrombosis, recurrent miscarriages and the stable presence of antiphospholipid antibodies (aPL). Circulating aPL can activate molecular mechanisms that may promote the activation of various cell types, particularly endothelial cells. Recently, endothelial activation has been associated with the release of pro-coagulant and pro-inflammatory extracellular microvesicles (EMV). This study analyzed the presence of EMV in the plasma of APS patients, their correlation with clinical manifestations, and their role in carrying antigenic targets and promoting endothelial cell activation. NanoSight analysis revealed that EMV concentrations were significantly more elevated in APS patients than in healthy donors. Moreover, we observed the presence of the main autoantigenic targets, β2-GPI and cardiolipin, on the surface of EMV from APS patients’ plasma, by both biochemical and flow cytometry analysis. It also revealed significantly higher cardiolipin levels on EMV from patients with obstetrical APS compared to those without pregnancy morbidity, specifically in women with a history of fetal death. To analyze the effect of the EMV from APS patients on endothelial cell activation and signaling, we then incubated in vitro human microvascular endothelial cells with patient-derived EMV, demonstrating a significant phosphorylation of IRAK, NF-κB, as well as increased expression and release of tissue factor. These findings suggest that circulating EMV may act as platforms for aPL binding and propagation of pathogenic immune complexes, introducing a new task to explain the immunoreactivity of the main antigenic targets of APS patients. Moreover, the presence of EMV may reflect disease features, but also actively participate in the pathogenesis, by triggering intracellular signaling pathways that sustain vascular inflammation and thrombosis.

FVIII-containing platelets modulate immune responses and attenuate inhibitor development in hemophilia A mice

2026-08-01T10:02:06+00:00

Development of inhibitory antibodies (inhibitors) against factor VIII (FVIII) is a significant complication of protein replacement therapy in hemophilia A (HA). Platelets (Plt), traditionally viewed as mediators of hemostasis, also modulate immune responses through cytokine release and interactions with immune cells. Harnessing these immunomodulatory properties may provide a novel strategy to prevent or suppress inhibitor formation. The object was to investigate whether FVIII-engineered Plt and related Plt-based products modulate FVIII immune responses in HA mice. FVIII-containing Plt were isolated from 2bF8 transgenic mice. FVIII-deficient mice were infused with intact FVIII-containing Plt, desialylated FVIII-containing Plt (dPlt), or acidified Plt lysates in combination with or before recombinant human FVIII (rhF8) exposure. Anti-FVIII antibody titers were determined by the Bethesda assay and enzyme-linked immunosorbent assay, and T-cell responses were analyzed by flow cytometry and proliferation assays. Co-infusion of FVIII Plt with rhF8 significantly reduced inhibitor titers compared with rhF8 alone. Acidified FVIII Plt lysates were potent, decreasing inhibitor titers by >20-fold when co-infused with rhF8. In contrast, co-infusion of dPlt with rhF8 did not suppress immune responses. However, repeated pre-sensitization with dPlt alone promoted immune tolerance to FVIII, evidenced by reduced inhibitor titers upon rhF8 immunization and attenuated CD4⁺ T-cell proliferation upon subsequent rhF8 exposure. These findings reveal a hierarchy of immune modulation, with intact Plt providing partial protection, lysates strongly suppressing immune responses, and dPlt inducing immune tolerance. FVIII-engineered Plt and Plt-derived products are potent immune modulators. These strategies offer novel and translatable approaches to both restore hemostasis and prevent or eradicate inhibitors in HA.

Increased percentages of circulating T follicular helper cells associate with disease subtype and activity in pediatric immune cytopenias

2026-08-01T10:02:41+00:00

Immune thrombocytopenia (ITP), warm autoimmune hemolytic anemia (wAIHA), and Evans syndrome (ES) have unpredictable disease activity and are sometimes associated with monogenetic disorders and/or extra-hematologic autoimmunity. ITP and immune neutropenia remain diagnoses of exclusion, hindering the diagnosis of ES in patients with multiple cytopenias. As there are no predictors of immunological comorbidities in these patients, it is difficult to determine who would benefit from genetic testing and/or evaluations for extra-hematologic autoimmunity. As circulating CD4+ T follicular helper (cTfh) cells promote autoimmunity, we quantified cTfh cells, associated clinical characteristics, and transcriptional signatures in a cohort of 153 pediatric patients with immune cytopenias (85 with ITP, 26 with wAIHA, and 42 with ES). cTfh cell percentages exceeding 9.5% had 76% sensitivity and 86% specificity for distinguishing ES from ITP or wAIHA, irrespective of disease activity, with a positive predictive value of 0.68 and negative predictive value of 0.91. Increased percentages of cTfh cells were associated with active cytopenia and decreased with treatment in patients with improving cytopenias over time, suggesting the utility of cTfh measurement for clinical monitoring. Increased percentages of cTfh cells were also associated with underlying immune disorders and extra-hematologic autoimmunity, thus identifying patients who would benefit from more extensive immunological evaluation. Single-cell RNA-sequencing of cTfh cells and plasma cytokines revealed increased interferon-α/β and interferon-γ signaling in patients with active wAIHA and ES, respectively. These results not only uncover immunological pathways differentiating subtypes of immune cytopenias, but also demonstrate applications of existing clinical tests in diagnosing immune cytopenias and in identifying patients who require more extensive evaluation for immunological comorbidities.

Mutational and copy number analysis at diagnosis and relapse of mantle cell lymphoma

2026-08-01T10:03:47+00:00

Most patients diagnosed with mantle cell lymphoma (MCL) experience extended remissions following frontline chemoimmunotherapy, yet with extended follow-up, relapses seem nearly inevitable. This study aimed to define the genomic landscape of MCL at diagnosis and relapse and investigate the clonal evolutionary dynamics associated with progression of disease (POD). We conducted comprehensive genomic sequencing on 214 tumor specimens from 189 patients, including 144 treatment-naïve and 70 POD samples, with 25 patients providing longitudinal paired samples pre-treatment and at POD. Comparative analyses were performed on single nucleotide variants, insertions/deletions and copy number alterations to assess genomic differences between specimens from treatment-naïve and relapsed patients. Additionally, mutational signatures were evaluated in pre-treatment samples, stratified by time to progression (≤24 months vs. >24 months). One hundred patients who received standard frontline chemoimmunotherapy were included in the survival analysis. Genomic profiles of pre-treatment specimens from patients who ultimately relapsed were strikingly similar to those observed in POD, while distinctly different from profiles associated with prolonged remissions. This genomic ‘stability’ was further confirmed by analysis of 25 paired specimens, demonstrating a remarkable genomic concordance despite extended remission periods (median >3 years), without a clear pattern of acquired alterations. Our findings suggest that MCL relapse is predominantly driven by pre-existing malignant clones at diagnosis, rather than by new evolutionary events, underscoring the importance of early detection and eradication of resistant clones to improve long-term outcomes.

EZH2 inhibition overcomes immunomodulatory drug resistance in multiple myeloma via a cereblon-dependent pathway

2026-08-01T10:05:41+00:00

Immunomodulatory agents (IMiD) and the next-generation cereblon (CRBN) E3 ligase modulators (CELMoD), targeting the IKZF1/IKZF3-IRF4-MYC axis, are effective therapies for multiple myeloma (MM) across all stages of disease. Resistance to treatment can be acquired following exposure, but a subset of patients has primary resistance, with both states necessitating the development of alternative treatment strategies. Enhancer of zeste homolog 2 (EZH2) has been shown to have increased expression at myeloma relapse and higher expression is associated with a shorter progression-free survival from diagnosis. EZH2 inhibitors have been studied as single agents in myeloma and in combination treatments to overcome drug resistance in other malignancies. In this study KMS-11 and RPMI-8226 myeloma cell lines were used as models of primary IMiD resistance, demonstrating persistent interferon regulatory factor 4 (IRF4) expression after IMiD/CELMoD exposure without loss of cell viability. The combination of tazemetostat, a Food and Drug Administration-approved EZH2 inhibitor, with IMiD/CELMoD significantly reduced IRF4 expression, induced apoptosis, and led to synergistic cell death in these resistant cell lines. Further investigations revealed that the synergistic effect of EZH2 inhibition appeared specific to IMiD/ CELMoD, was CRBN-dependent and was rescued by IRF4 overexpression. Mechanistically, tazemetostat appeared to reduce IKZF1 binding to the IRF4 promoter and super-enhancer, explaining how the combination with IMiD/CELMoD which also have this effect may reach the threshold required to suppress IRF4 expression and ultimately inhibit MM cell growth in resistant cell lines. Our findings highlight a potential strategy for treating MM patients with IMiD resistance.

Male sex adversely impacts survival and myeloid malignancy risk in MGUS: a real-world population-based study

2026-08-01T10:06:42+00:00

Monoclonal gammopathy of undetermined significance (MGUS) is a common plasma cell disorder with well described risks of progression to myeloma and lymphoplasmacytic lymphoma. Using data from an established UK population-based cohort of hematological malignancies and premalignancies, we investigated patient and disease characteristics, subsequent hematological malignancy, and survival in 4,651 people diagnosed with MGUS between 2005 and 2019. The 5-year net (relative) survival (disease-specific estimate of the probability of survival) for MGUS patients was 87.8% (95% confidence interval [CI]: 85.9-89.7), with males (83.8%; 95% CI: 81.0-86.6) more affected than females (92.2%; 95% CI: 89.7-94.7). The proportion of subsequent hematological malignancies was also higher in males than females (8.8% vs. 5.3%; P<0.00001); the average annual rates of transition being 1.81% (95% CI: 1.44-2.18) and 0.99% (95% CI: 0.72-1.27), respectively. Furthermore, whilst annual rates of transformation to myeloma (1.04%) and lymphoplasmacytic lymphoma (0.11%) were as expected, both were higher in males (1.23% and 0.18%) than females (0.87% and 0.06%). With a median time to diagnosis of 40 months, the incidence of myeloid malignancy was also raised in males (relative risk=3.6; 95% CI: 2.5-4.9), but not females (relative risk=1.0; 95% CI: 0.3-1.9). No associations between MGUS and subsequent development of chronic lymphocytic leukemia were observed. Providing new data on the nature of MGUS progression, our analyses revealed previously undescribed sex disparities; including worse survival and increased rates of myeloid malignancy in males with non-IgM MGUS. These findings have implications for future research, as well as risk stratification and monitoring of patients with this highly prevalent plasma cell dyscrasia.

RAP1-RHO small GTPase cross-talk mediates integrindependent and -independent platelet procoagulant response

2026-08-01T10:07:03+00:00

Platelet adhesion and procoagulant activity are critical for primary and secondary hemostasis, respectively. The small GTPase RAP1 is a central regulator of platelet aggregation as it controls αIIbβ3 integrin activation through direct interaction with the integrin adapter protein, TALIN1 (TLN1). In addition to their aggregation defect, activated platelets lacking RAP1 (Rap1mKO) exhibited a marked impairment in surface exposure of phosphatidylserine (PtdSer), a negatively charged phospholipid with procoagulant activity. However, the mechanisms by which RAP1 regulates PtdSer exposure are unclear. Here we investigated the hypothesis that RAP1 regulates platelet PtdSer exposure through cross-talk with small GTPases of the RHO family. Consistent with their defect in PtdSer exposure, Rap1mKO platelets showed reduced procoagulant activity in vitro and in vivo when compared to controls. Stimulated Rap1mKO platelets exhibited elevated RHOA-GTP levels, and inhibition of the RHOA effector, Rho associated coiled-coil kinase (ROCK), partially restored PtdSer exposure in these cells. A milder defect in PtdSer exposure was observed for platelets from Tln1mR35/118E mice, i.e., mice with impaired RAP1-TLN1 interaction but otherwise intact RAP1 signaling. ROCK inhibition fully restored PtdSer exposure in Tln1mR35/118E platelets. Opening of the mitochondrial permeability transition pore, a cellular response critical to PtdSer exposure, was impaired in Rap- 1mKO platelets and restored by pretreatment of cells with the ROCK inhibitor. Our study provides first evidence that platelet RAP1 signaling affects hemostatic plug formation independent of its key role in platelet adhesion. Additionally, our studies strongly suggest that RAP1 regulates PtdSer exposure and procoagulant activity in a RHOA/integrin-dependent and -independent manner.

Genetic and clinical characteristics of 54 pediatric lymphoma patients with variant mutation sites of UNC13D

2026-08-01T10:07:18+00:00

High-cholesterol diet fuels myeloma progression, dysregulates adipokine expression in vivo, and impairs treatment response ex vivo

2026-08-01T10:07:46+00:00

Body mass index during and early after therapy for pediatric acute lymphoblastic leukemia is associated with obesity in survivors

2026-08-01T10:08:22+00:00

Cumulative incidence and factors associated with subsequent myeloid neoplasms in patients with nodal T-follicular helper cell lymphomas

2026-08-01T10:09:15+00:00

CD19-directed CAR T therapy for intravascular large B-cell lymphoma

2026-08-01T10:10:38+00:00

FLAG-IDA-venetoclax for high-risk newly diagnosed acute myeloid leukemia: a multicenter real-world study

2026-08-01T10:11:16+00:00

Extramedullary hematopoiesis in the spleen contributes to natural killer cell development during infection and inflammation

2026-08-01T10:11:43+00:00

Morphologic and immunophenotypic characterization of lymphocytosis following BCMA-targeted CAR-T cell therapy in relapsed/refractory multiple myeloma

2026-08-01T10:11:54+00:00

Three-year safety, efficacy, and renal outcomes of mitapivat treatment in sickle cell disease: results from the phase 2 open-label study

2026-08-01T10:11:59+00:00

GB2064 (lenumlostat) shows preliminary evidence of bone marrow collagen fibrosis reduction with manageable tolerability in JAK inhibitor-refractory myelofibrosis: results from the MYLOX-1 phase IIa study

2026-08-01T10:12:06+00:00

Bleomycin omission in limited-stage classic Hodgkin lymphoma with negative PET scan after two cycles of ABVD

2026-08-01T10:12:09+00:00

Histological response dynamics in gastric extranodal marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue after Helicobacter pylori eradication: a single-center longitudinal analysis

2026-08-01T10:12:12+00:00

Scott syndrome with novel compound heterozygous pathogenic variants in ANO6 and reduced thrombin generation

2026-08-01T10:12:13+00:00

Ruxolitinib in treatment-naive or corticosteroid-refractory pediatric patients with chronic graft-versus-host disease: final analysis of the phase II REACH5 trial

2026-08-01T10:12:17+00:00

No increased risk of acute myeloid leukemia in adults with primary immune thrombocytopenia treated with thrombopoietin receptor agonists: a French nationwide population-based study

2026-08-01T10:12:20+00:00

A nationwide Italian GIMEMA survey on tandem autologous stem cell transplantation for newly diagnosed multiple myeloma patients treated with daratumumab, bortezomib, thalidomide and dexamethasone

2026-08-01T10:12:21+00:00

Mutual amplification of sensory nerve outgrowth and tumor progression in myeloma

2026-08-01T10:12:26+00:00

Real-world outcomes of newly diagnosed multiple myeloma patients treated with front-line daratumumab bortezomib lenalidomide and dexamethasone

2026-08-01T10:12:29+00:00

Nationwide analysis of acute promyelocytic leukemia: incidence and patient outcomes in Germany

2026-08-01T10:12:32+00:00

Intensive induction therapy with FLAG-idarubicinvenetoclax for fit older high-risk patients with acute myeloid leukemia

2026-08-01T10:12:35+00:00

An unusual case of basophilic meningitis revealing a chronic-phase chronic myeloid leukemia: a report after almost three years of follow-up

2026-08-01T10:12:36+00:00

Immune effector cell-associated hemophagocytic lymphohistiocytosis-like syndrome during treatment with the bivalent CD20xCD3 bispecific antibody glofitamab

2026-08-01T10:12:39+00:00

Clinical and therapeutic impact of newborn screeningbased early detection of ataxia-telangiectasia

2026-08-01T10:12:41+00:00

Rare dual-clone phenomenon: concurrent λ AL amyloidosis and κ restricted B-cell lymphoproliferative disorders

2026-08-01T10:12:42+00:00

Erratum to: “A simplified frailty score predicts outcome in curatively treated older patients with classical Hodgkin lymphoma”

2026-08-01T20:04:33+00:00

Erratum to: “Tumor burden-guided dosing contributes to mitigation of immunotoxicities following treatment with obecabtagene autoleucel in adult patients with relapsed/ refractory B-cell acute lymphoblastic leukemia”

2026-08-01T20:04:33+00:00