Haematologica

The JAK2 V617F revolution in myeloproliferative neoplasms

Ayalew Tefferi — Sun, 01 Nov 2026 00:00:00 +0000

What’s liver got to do with it? Hepatic response and survival in AL amyloidosis

Jeffrey A. Zonder — Thu, 16 Jul 2026 00:00:00 +0000

Mind the gap: anti–PD-1 salvage before autologous transplantation in classical Hodgkin lymphoma

Daniel Noerenberg — Thu, 12 Mar 2026 00:00:00 +0000

GATA2 coming of age: 15 years from discovery to symptoms

Lili Kotmayer, Marcin W. Wlodarski — Thu, 11 Jun 2026 00:00:00 +0000

Prime salvage treatment for pediatric acute myeloid leukemia

Gertjan J.L. Kaspers — Thu, 18 Jun 2026 00:00:00 +0000

Refining post-blinatumomab risk stratification through ultrasensitive-based measurable residual disease assessment

Yazeed Samara, Ibrahim Aldoss — Thu, 16 Apr 2026 00:00:00 +0000

Rooted in reality, living with hope: post-treatment fertility preservation

Rebecca K. Chung, Vivian G. Oehler — Thu, 18 Jun 2026 00:00:00 +0000

The expanding spectrum of CAR-T related T-cell lymphomas

Theresa Schönrade, Till Braun — Thu, 12 Mar 2026 00:00:00 +0000

Prognosis in marginal zone lymphoma: a comprehensive review

Thu, 05 Mar 2026 00:00:00 +0000

Marginal zone lymphomas (MZL) represent a distinct subset of indolent B-cell lymphomas, including extranodal, nodal, and splenic variants. Despite shared histopathological and immunophenotypic features, their clinical presentation varies significantly based on the site of origin and genetic abnormalities. The heterogeneity of the disease is reflected in its management, particularly in therapeutic strategies and prognosis determination. Several prognostic tools have been developed to refine risk assessment in MZL subtypes, including the Mucosa-Associated Lymphoid Tissue International Prognostic Index, the Hemoglobin Platelets Lactate Dehydrogenase Lymphadenopathy score and its simplified version. Recently, the Marginal Zone Lymphoma International Prognostic Index has emerged as a comprehensive model integrating data from all MZL subtypes and incorporating rigorously validated clinical parameters. This review aims to synthesize current knowledge on MZL prognosis, critically assess existing prognostic models, and highlight the potential clinical impact of achieving risk stratification.

Reframing leukemia-niche interactions: the emerging role of the marrow adipocyte lineage

Thu, 02 Jul 2026 00:00:00 +0000

The bone marrow is a highly dynamic organ that undergoes continuous remodeling to maintain all different hematopoietic cell populations throughout life, adapting during development, aging, and disease. It serves as the primary site of both normal hematopoiesis and leukemic initiation and progression. While mesenchymal stromal cells have received substantial attention for their contribution to support acute leukemia, the bone marrow adipocyte lineage has remained largely overlooked. There are two main reasons for this: first, adipogenic progenitors are typically grouped under the broad mesenchymal stromal cell umbrella, obscuring the distinct contributions of specific stromal subsets; second, mature bone marrow adipocytes have traditionally been regarded as inert energy reservoirs rather than active components of the marrow microenvironment. Recent evidence challenges this view, demonstrating that different types of adipocyte lineage cells actively promote acute leukemia progression and chemotherapy resistance through distinct mechanisms. In this review, we summarize recent advances in defining subpopulations within the bone marrow adipocyte lineage and outline how leukemic cells exploit their functions. We further discuss how standard chemotherapy may inadvertently reshape leukemic–adipocyte lineage interactions, mediating resistance and facilitating the re-emergence of disease.

Recovering from a therapeutic stall in higher-risk myelodysplastic syndromes: re-examining biology, backbones and study designs

Sudhir Tauro, Ayalew Tefferi — Thu, 23 Apr 2026 00:00:00 +0000

Therapeutic progress in higher-risk myelodysplastic syndromes (HR-MDS) has stalled. Despite repeated attempts to improve outcomes through incremental refinements to classification systems and hypomethylating agent (HMA)-based backbones, no phase III study since AZA-001 has replicated even the modest survival benefit observed with azacitidine. We propose that this stagnation results from a fundamental mismatch between the biological realities of HR-MDS and the assumptions underpinning contemporary drug development. HR-MDS encompasses biologically diverse ecosystems characterized by distinct clonal architectures, evolutionary trajectories and marrow microenvironmental dysfunction, despite overlapping phenotypic and genotypic features. Treating this heterogeneity as a single entity anchored to a HMA backbone, risks obscuring therapeutic signals and misinterpreting responses. Here, we examine the potential biological, microenvironmental, and methodological drivers of therapeutic insufficiency in HR-MDS, to advocate for biologically coherent adaptive platform trials using biomarker-enriched selection of patients, and propose shifting away from default HMA backbones. Only by redesigning strategy around biology, rather than prioritizing ease of recruitment, or historical precedent, can we restore momentum and lift in HR-MDS drug development.

Multicenter prospective phase II study of decitabine priming with low-dose idarubicin, cytarabine, and G-CSF in children with refractory or relapsed acute myeloid leukemia

Thu, 05 Feb 2026 00:00:00 +0000

There is no standard salvage regimen for relapsed/refractory (R/R) pediatric acute myeloid leukemia (AML). In this prospective, multicenter phase II trial, 101 evaluable patients (<18 years) received one course of decitabine priming followed by low-dose idarubicin, cytarabine, and G-CSF (DP-IAG) as remission reinduction therapy. The primary objective was the rate of complete remission, including incomplete hematologic recovery (CR/CRi). Seventy-four patients (73.3%; 95%CI: 64.6-81.9%) achieved CR/CRi. Ultimately, 70 patients (69.3%) underwent allogeneic hematopoietic stem cell transplantation (alloHSCT). At a median follow-up of 36.4 months (Interquartile Range: 10.3–51.3), the estimated 3-year overall survival for the entire cohort was 60.8% (95%CI: 55.9-65.7%). Infections were the most frequent non-hematologic adverse events; 3 patients died from toxicity after the first reinduction. DP-IAG demonstrated high remission rates and an acceptable safety profile, supporting its use as an effective salvage option and feasible bridge to HSCT. These findings provide a benchmark for future trials in pediatric R/R AML.

Establishing reverse chimeric antigen receptor T cells for precise targeting of immune-mediated thrombotic thrombocytopenic purpura

Thu, 16 Apr 2026 00:00:00 +0000

Immune-mediated thrombotic thrombocytopenic purpura (iTTP) is a life-threatening autoimmune disorder caused by autoantibodies that target the metalloprotease ADAMTS13. This prevents the cleavage of ultra-large von Willebrand factor (UL-VWF), thereby forming microthrombi in the microvasculature. While current treatments are effective, ADAMTS13 relapses occur in up to 15% of the patients after rituximab administration. In this study, we propose a novel approach addressing the unmet need for treatment of patients with ADAMTS13 refractoriness and for patients requiring repeated treatment. Our strategy involves developing two targeted therapies that aim to achieve highly effective and safe B-cell depletion. For the first time, we employ adapter chimeric antigen receptor (CAR) T cells called reverse CAR (RevCAR) T cells to (i) achieve a broader and deeper B-cell depletion by targeting CD19 and (ii) selectively deplete the disease-causing anti-ADAMTS13 autoreactive B cells to increase precision and safety in iTTP treatment. Therefore, we have developed novel target modules (RevTM) against CD19+ and anti-ADAMTS13 autoreactive B cells. We show that the RevCAR T cells successfully and specifically kill target hybridomas and Nalm-6 cells in a RevTM-dependent manner and at low effector- to-target cell ratios. Moreover, the RevCAR T cells are able to eliminate the target cells even in the presence of high concentrations of ADAMTS13 autoantibodies. Overall, our findings demonstrate for the first time, a proof-of-concept that anti-ADAMTS13 autoreactive B cells can be selectively depleted by the RevCAR T-cell platform paving the way for an effective and safe therapy for iTTP.

Cyp7b1-inhibiting azoles enhance hematopoietic stem and progenitor cell mobilization in normal and sickle cell disease mice

Thu, 09 Apr 2026 00:00:00 +0000

Mobilized hematopoietic stem and progenitor cells (HSPC) are essential for transplantation-based therapies, including curative gene therapies for sickle cell disease (SCD). While granulocyte colony-stimulating factor (G-CSF, filgrastim) remains the standard mobilization agent, many patients respond inadequately, and it can trigger life-threatening vaso-occlusive crises in SCD. The CXCR4 antagonist AMD3100 (plerixafor) is routinely combined with G-CSF for non-SCD settings but is ineffective as a single agent in SCD, underscoring the urgent need for alternative strategies. We previously identified 27-hydroxycholesterol (27HC) as a physiological inducer of HSPC mobilization during pregnancy. Here, we show that exogenous 27HC enhances AMD3100-induced HSPC mobilization in mice, either alone or with G-CSF. Because 27HC is metabolized by the enzyme Cyp7b1, we tested whether pharmacological Cyp7b1 inhibition could mimic this effect. Treatment with clotrimazole, an antifungal and Cyp7b1 inhibitor, significantly enhanced AMD3100-induced HSPC mobilization in wild-type, SCD, and humanized mice. Importantly, intravenous administration of voriconazole, a clinically approved systemic antifungal with Cyp7b1-binding activity, similarly augmented AMD3100-induced HSPC mobilization in wild-type and SCD mice without altering steady-state hematopoiesis. These findings establish Cyp7b1-inhibiting azoles as novel and clinically relevant enhancers of HSPC mobilization, particularly for SCD patients who cannot safely receive G-CSF but require robust HSPC yields for gene therapy.

Anti–programmed cell death protein 1–based salvage therapy for relapsed/refractory Hodgkin lymphoma: a multicenter real-world analysis

Thu, 26 Feb 2026 00:00:00 +0000

In relapsed/refractory classic Hodgkin lymphoma (r/r cHL), salvage followed by high-dose chemotherapy and autologous stem cell transplantation (HD-ASCT) yields suboptimal outcomes. Programmed cell death-1 (PD-1) inhibitor-based salvage regimens have shown superior complete response (CR) rates of up to 95% (for the P-GVD regimen) with unprecedented progression-free survival (PFS) after HD-ASCT. However, immune checkpoint inhibitors are not approved by the European Medicines Agency in second-line treatment, and European data remain sparse. This retrospective, multicenter analysis included r/r cHL patients who received salvage with intent to consolidation. Responses before and after stem cell transplant consolidation, and PFS and overall survival (OS) were assessed. Forty-seven patients were included (median prior lines: of therapy 2). Salvage regimens were PD-1 monotherapy (N=10), PD-1 + chemotherapy (P-ICE/N-ICE/P-GVD) (N=34), or PD-1 + BV (brentuximab vedotin) (N=3). Overall response (OR)/CR rates were 90.9%/47.7%. OR/CR rates by salvage regimen were: PD-1 monotherapy 80%/10%; PD-1 + chemotherapy, 93.6%/61.3%; PD-1 + BV, 100%/33.3%. With a median follow-up of 16 months, 1-year PFS was 83.9% and OS was 95.6%. In the subgroup of patients who had received one prior line of therapy (N=22), 1-year PFS was 100%. In this real-world cohort, previously reported high CR rates were not reached. However, with the restriction of a limited follow-up, outcomes after HDASCT were excellent, supporting the role of PD-1 inhibitor-based salvage followed by consolidative HD-ASCT for r/r cHL.

Risk of fractures according to iron parameters and hemochromatosis HFE genotype in 142,146 general population individuals

Thu, 26 Mar 2026 00:00:00 +0000

The risk of fractures may be increased in individuals with iron deficiency, iron overload, and/or HFE hemochromatosis. To test this hypothesis, we followed 142,146 individuals from the Danish general population for a median of 11 years (range, 0-41) after study enrollment for hospital and emergency room admissions with fractures. All individuals had blood samples drawn at study enrollment. We measured iron, transferrin saturation, and ferritin in 136,611, 136,555, and 37,990 individuals, respectively, while 132,499 individuals were genotyped for the HFE C282Y and H63D variants. We found a U-shaped relationship between fracture risk and concentration of plasma iron and transferrin saturation when studying all individuals irrespective of genotype. When studied according to plasma ferritin concentration, fracture risk was increased in individuals with low ferritin concentrations, while risk was not increased in individuals with high concentrations. When compared to non-carriers, HFE C282Y homozygotes had an increased risk of any fracture (hazard ratio [HR]=1.38; 95% confidence interval [95% CI]: 1.09-1.75; P=0.008), and risk was increased even in C282Y homozygotes with normal ferritin concentrations (HR=2.89; 95% CI: 1.50-5.56), which is important as these individuals would not usually be recommended for HFE genotyping according to clinical guidelines. When compared to risk in non-carriers, risk of fracture of the hip and femur was increased in C282Y homozygotes (HR=1.78; 95% CI: 1.17-2.70; P=0.007) but surprisingly also in H63D homozygotes (HR=1.21; 95% CI: 1.00-1.47; P=0.04), C282Y heterozygotes (HR=1.10; 95% CI: 1.00-1.21; P=0.04), and C282Y/H63D compound heterozygotes (HR=1.23; 95% CI: 1.00-1.51; P=0.05). The markedly increased fracture risk in C282Y homozygotes with normal ferritin may challenge the presumption that systemic iron accumulation is the primary mechanism causing these individuals increased fracture risk. Further studies are needed to examine whether phlebotomy reduces fracture risk.

GATA2 at 14: genotype-phenotype correlations

Thu, 15 Jan 2026 00:00:00 +0000

GATA2 mutations cause adult-onset bone-marrow failure characterized by cytopenias, infections and increased risk of myeloid malignancy. We reviewed hospital records and referrals of 232 GATA2-mutated individuals from 122 families to gather hematopoietic and syndromic features. Mutations were categorized by their effect on GATA2 protein: mutation after the second zinc-finger (C-term, N=10); missense in the second zinc-finger (ZF2, N=104); mutations producing a stable truncated protein (Truncation, N=22); Null alleles (mRNA instability, large deletions, N=46); or Enhancer mutations (N=50). Regression models for symptom onset identified earlier onset and increased hazard ratios (HR) between Truncation, Null or ZF2 mutations (13 years, HR=5.00; 17 years, HR=3.60; and 22 years, HR=2.23, respectively) and Enhancer mutations. Commonly mutated ZF2 amino acids also stratified patients: those with R396 or T354 presented earlier with increased hazard ratios (16 years, HR=2.96 and 19 years, HR=2.16, respectively) compared to those with R398 (34 years). Mutation groups with a median onset before 20 years had higher prevalences of cytopenias, infections, human papilloma virus (HPV), thromboses and hearing loss. Warts/anogenital HPV were common (93/232, 40.1%). Non-hematologic manifestations included hearing loss (45/232; 19.4%), lymphedema (30/232; 12.8%), and non-hematologic malignancies (46/232, 19.8%), the majority being HPV-related anogenital cancers. Leukemia or lymphoma occurred in 25/232 patients (10.8%). Functional analysis of patients’ mutations showed impaired transactivation. Males had more monosomy 7 (17/73 males, 6/110 females, P=0.0016). Non-tuberculous mycobacterial infection was the presenting symptom in 14/73 males versus 7/110 females (P=0.0151). GATA2 mutation type and specific mutations affect penetrance and expression. Sex is an independent risk for specific infectious presentations and cytogenetic abnormalities. ClinicalTrials.gov identifier: NCT01905826.

Immune evasion in primary central nervous system lymphoma: macrophage and T cell roles in response to immunotherapy

Thu, 23 Apr 2026 00:00:00 +0000

Primary central nervous system (CNS) lymphoma is an aggressive extranodal lymphoma with poor prognosis, largely due to its capacity for immune evasion within the unique microenvironment of the CNS. Here, we investigated the interactions between macrophages and T cells in a syngeneic mouse model of primary central nervous system lymphoma (PCNSL), manipulating macrophage/microglia populations and MHC class I expression on tumor cells to mimic patient-associated immune escape. We found that macrophages and microglia are indispensable for anti-tumor immunity and significantly enhance the efficacy of PD1 checkpoint blockade, particularly when tumor cells retain MHC-I expression. In contrast, depletion of these myeloid cells led to accelerated disease progression and diminished response to immunotherapy, highlighting the importance of both innate and adaptive immunity in PCNSL. Interestingly, MHC-I-deficient PCNSL did not respond to T-cell-based therapies and was controlled exclusively by macrophages, rendering prognosis largely dependent on this alteration. Our findings support the need for therapeutic strategies that target both T-cell and myeloid compartments and suggest that profiling MHC-I expression may help guide personalized immunotherapy approaches in this challenging disease.

Lenalidomide-rituximab or lenalidomide-rituximabbendamustine for relapsed/refractory follicular lymphoma: primary and final analysis of the randomized phase II HOVON110/ReBeL study

Thu, 16 Apr 2026 00:00:00 +0000

The R² (lenalidomide-rituximab) and R² with bendamustine (R²B) regimens are both feasible in relapsed/refractory follicular lymphoma (R/R FL), but prospective phase II data on R²B are lacking. In this multinational, prospective, randomized, non-comparative trial, patients with R/R FL were randomized 1:1 to R² (arm A) or R²B (arm B). Patients achieving computed tomography-based partial or complete remission (PR/CR) received rituximab maintenance every 3 months for 2 years. Co-primary endpoints were investigator-assessed CR rates at end-of-induction (EOI) and severe toxicity rates. Between December 2014 and July 2019, 92 patients were randomized. The trial was stopped prematurely due to slow accrual. CR rates at EOI were 11.4% (95% confidence interval [CI]: 3.8-24.6%) for R2 and 15.2% (95% CI: 6.3-28.9%) for R2B. With a median follow-up of 74 months, predefined severe toxicities occurred in three (6.8%; 95% CI: 1.4-18.7%) and six patients (13.0%; 95% CI: 4.9-26.3%) in arm A and arm B respectively, with two pneumonia-related deaths in arm A and no treatment-related deaths in arm B; 43% and 66% experienced any grade 3-4 adverse events (2%/7% grade 4). At 60 months, in arms A and B event-free survival was 39.5% (95% CI: 25.1-53.6%) and 56.4% (95% CI: 40.1-69.3%). Overall survival was excellent at 72.1% and 86.3%, respectively. R² and R²B are both effective treatment regimens for R/R FL. While computed tomography-based CR rates were low, treatment with R²B resulted in numerically longer median event-free survival and overall survival, but this was associated with higher toxicity.

Effect of intravenous immunoglobulin on infections in multiple myeloma patients receiving daratumumab

Thu, 23 Apr 2026 00:00:00 +0000

Daratumumab is an anti-CD38 monoclonal antibody that has shown clinical benefit in both relapsed/refractory as well as newly diagnosed multiple myeloma (MM). Although daratumumab is very well-tolerated, randomized clinical trial data have consistently demonstrated an increased risk of infection, particularly along the respiratory tract, in patients receiving daratumumab. CD38 is present on healthy plasma cells, and their destruction can lead to hypogammaglobulinemia (HGG). In this study, we retrospectively reviewed all patients with MM treated with daratumumab and intravenous immunoglobulin (IVIG) at our institution from 2015-2019. The primary endpoints were the incidence rate ratios (IRR) of all-grade infections and grade 3-4 infections per patient-year during IVIG versus observation. In addition, a separate reference group of MM patients who were treated with daratumumab but never received IVIG was identified to establish baseline infection rates and to identify differences in baseline characteristics among patients who were selected to receive IVIG. A total of 43 patients received daratumumab and IVIG, primarily in the relapsed/refractory setting. All patients had HGG during treatment with daratumumab, with most (81%) experiencing moderate HGG (IgG <400 mg/dL). During periods of IVIG use, all-grade infections were 43% lower and grade 3-4 infections were 70% lower compared to observation periods (no IVIG use). The reference group that had never received IVIG (N=100) had fewer infections in the year prior to daratumumab and a lower infection rate while on daratumumab. In conclusion, selected patients with multiple recurrent infections prior to starting daratumumab derived substantial benefit from the use of IVIG.

Hepatic response criteria in light chain amyloidosis: a multicenter validation study

Thu, 15 Jan 2026 00:00:00 +0000

Liver involvement in light chain amyloidosis (AL) is seen in 10-20% of patients and is associated with poor prognosis. The goal of this study was to assess the prognostic impact of the hepatic response criteria. AL patients diagnosed between 2010 and 2015 with liver involvement (serum alkaline phosphatase [AP] >1.5 upper reference limit (URL)] who achieved a hematologic response were included. Hepatic response was defined as >50% reduction (or normalization) of AP from baseline. Hepatic response was assessed at 6, 12, and 24 months after therapy initiation and at best response. Overall survival was assessed from time of therapy initiation. Hepatic response was evaluated in 116 patients. The median baseline serum AP was X2.6 URL. Hematologic very good partial response or better (≥VGPR) was achieved in 69% of patients. AP decreased with time, with a median reduction of 22%, 34%, and 53% at 6, 12, and 24 months, respectively, and a median AP reduction of 56% at the time of best response. The median time to hepatic response was 13.3 months and was longer for patients undergoing autologous stem cell transplantation. Achievement of hepatic response, particularly as early as 12 months, and at best response, was associated with improved survival, independently of other prognostic factors. Predictors of hepatic response include higher baseline AP level, lower total bilirubin, hematologic ≥VGPR, and cardiac and renal responses, when applicable. Hepatic response measured by the change in AP is a prognostic factor in patients with AL amyloidosis.

The genetic landscape of extramedullary plasmacytoma: a comparative analysis with extramedullary disease of multiple myeloma

Thu, 09 Apr 2026 00:00:00 +0000

Extramedullary (or extraosseous) plasmacytoma (EMP) is a localized plasma cell neoplasm lacking apparent bone marrow involvement and other features of multiple myeloma (MM). The prognosis is usually favorable and progression to MM is infrequent. The genetic landscape of EMP remains largely unknown. Importantly, EMP must be distinguished from extramedullary disease of MM (EMD), which typically exhibits an aggressive behavior. We performed a comprehensive molecular analysis of EMP (N=24) in comparison to EMD (N=24) using fluorescence in situ hybridization, copy number profiling, and targeted next-generation sequencing. Overall, EMP shared several genetic features with MM, but exhibited markedly lower complexity than EMD. EMP revealed a mean of 4.3 copy number changes versus 19.3 in EMD (P<0.001). IGH breaks were detected in six EMP and ten EMD, and hyperdiploidy in ten and 14 cases, respectively. Gains of 1q21 occurred in nine EMP and 15 EMD (P=0.045). Likewise, EMP harbored fewer mutations (median 2.0 vs. 3.0; P<0.01), yet was enriched for TRAF3 mutations, detected in six cases, which were absent in EMD (P=0.022). In contrast, EMD more frequently harbored mutations associated with advanced MM, including NRAS/KRAS (P<0.01), TP53, TENT5C, ARID1A, and ATM. In conclusion, we demonstrate that EMP shows a significantly less complex and, in part, distinct genetic profile compared to EMD. This may aid in differentiating the two entities in diagnostically challenging cases and could help to identify EMP with an increased risk of progression.

Prevalence and impact of frailty assessed using standard geriatrics tools in older adults with blood cancers

Thu, 23 Apr 2026 00:00:00 +0000

Geriatric assessment is recommended for older adults undergoing cancer treatment, but the best frailty assessment tools for blood cancers have still not been identified. We conducted a prospective cohort study of three gold standard approaches: the cumulative deficit index, phenotypic frailty, and 4-meter gait speed. From February 2015 to January 2025, a research assistant approached patients aged ≥73 years attending new consultations for leukemia, lymphoma, and multiple myeloma. A total of 1,011 patients underwent frailty assessment with a median age of 78 years (interquartile range [IQR]: 76-82 years) and a median follow-up among survivors of 43 months (IQR: 18-74 months). For example, when classified by phenotypic frailty, 11% were frail, 59% pre-frail, and 30% robust; using this tool, frail patients lived 24 months compared to 92 months among robust patients. While frailty classification varied across measures, all three tools were associated with mortality in a dose-dependent manner, independent of age and sex (cumulative deficit index: ref=robust; pre-frail HR 1.86 [95%CI: 1.54, 2.26]; frail HR 2.42 [1.85, 3.17]; phenotypic frailty: ref=robust; pre-frail HR 1.88 [1.50, 2.37], frail HR 3.01 [2.22, 4.07]); gait speed: ref=≥0.8 m/s; 0.6 to <0.8 m/s HR 1.44 [1.18, 1.76], <0.6 m/s HR 2.06 [1.61, 2.63]). Associations were similar when analyzed by disease clinic; cumulative deficit further stratified risk in patients assessed by phenotypic frailty and gait speed. Our findings provide a new benchmark on frailty and its impact on survival in older adults with blood cancers, with care delivery implications for operationalization in clinical practice and research.

Survival assessment of warfarin and international normalized ratio exposure in cancer-associated venous thromboembolism: Veterans Affairs healthcare systembased analysis

Thu, 02 Apr 2026 00:00:00 +0000

Venous thromboembolism (VTE) is a common complication among patients with cancer. While randomized clinical trials have established the safety and efficacy of direct oral anticoagulants (DOAC) and low-molecular-weight heparin (LMWH) relative to warfarin for the treatment of cancer-associated thrombosis, emerging evidence suggests that warfarin may be associated with improved overall survival in patients with malignancy. We evaluated survival outcomes among patients with cancer and VTE treated with warfarin compared with other anticoagulants within the Veterans Affairs (VA) Healthcare System and analyzed the association of international normalized ratio (INR) exposure and overall survival. Among 12,298 propensity-matched patients (mean age 69 years; 97% men), warfarin use was associated with a 16% lower risk of mortality compared with other anticoagulants (hazard ratio [HR]=0.84; 95% confidence interval [CI]: 0.80-0.88; P <0 .001). Median survival was 1,457 days in the warfarin group versus 1,045 days in the non-warfarin group. Survival benefits were consistent across subgroups defined by tumor type, stage, and demographic characteristics. In landmark analyses, the greatest benefit was observed with extended periods in the INR range of 2.5 to 3.0 (HR=0.81; 95% CI: 0.75-0.87). In this population-based cohort study of patients with cancer and VTE, warfarin use was associated with improved survival compared with other anticoagulants. The greatest benefit was observed among patients who maintained an INR between 2.5 and 3.0.

Efficacy of the kinase inhibitor CHZ868 against JAK2 rearrangements in pediatric acute lymphoblastic leukemia

Thu, 16 Apr 2026 00:00:00 +0000

Anti-CD19 CAR T-cell therapy in relapsed/refractory T-cell/ histiocyte-rich large B-cell lymphoma: insights from the French DESCAR-T registry, a LYSA study

Thu, 09 Apr 2026 00:00:00 +0000

Gene expression profile of adult T-cell leukemia/lymphoma with human T-cell lymphotropic virus type 1-infected Hodgkin and Reed-Sternberg-like cells is more similar to classic Hodgkin lymphoma than typical adult T-cell leukemia/lymphoma

Thu, 16 Apr 2026 00:00:00 +0000

Impact of high-sensitivity next-generation sequencing measurable residual disease and subsequent stem cell transplant in patients receiving blinatumomab for MRDpositive B-cell acute lymphoblastic leukemia

Thu, 26 Mar 2026 00:00:00 +0000

Allograft inflammatory factor-1 is essential for acute monocytic leukemia infiltration

Thu, 23 Apr 2026 00:00:00 +0000

Acceptability and feasibility of post-treatment fertility preservation in women previously treated for hematological diseases

Thu, 02 Apr 2026 00:00:00 +0000

Changes in neutrophil-to-lymphocyte ratio in patients with polycythemia vera treated with ruxolitinib reflect JAK2 variant allele frequency

Thu, 09 Apr 2026 00:00:00 +0000

Pre-treatment circulating microRNA signatures predict outcomes of anti-CD19 CAR T-cell therapy

Thu, 23 Apr 2026 00:00:00 +0000

Novel KAT6B::NUTM2B fusion oncogene in congenital acute myeloid leukemia and implications for menin inhibitor therapy

Thu, 23 Apr 2026 00:00:00 +0000

Local cytokine release syndrome with cervical angioedema following CAR-T cell therapy

Thu, 23 Apr 2026 00:00:00 +0000

Favorable safety and efficacy profiles of α-1-antitrypsin in steroid- and ruxolitinib-refractory acute graft-versus-host disease of the gastrointestinal tract: a retrospective, single center study

Thu, 23 Apr 2026 00:00:00 +0000

Phase Ib/II trial of anti-CD33 monoclonal antibody BI 836858 and azacitidine in previously untreated older acute myeloid leukemia patients: Beat AML S2 sub-study results

Thu, 23 Apr 2026 00:00:00 +0000

Venetoclax and gilteritinib combination for FLT3-mutated relapsed/refractory acute myeloid leukemia: a real-world single-center experience

Thu, 07 May 2026 00:00:00 +0000

SWI/SNF alterations define a subgroup with poorer outcome among patients with aggressive forms of adult T-cell leukemia/lymphoma

Thu, 07 May 2026 00:00:00 +0000

Origins of iAMP21 in children who later developed pediatric acute lymphoblastic leukemia: an investigation of neonatal blood spots

Thu, 16 Apr 2026 00:00:00 +0000

Pediatric blastic plasmacytoid dendritic cell neoplasms are molecularly defined by recurrent MYB rearrangements: clinical and molecular insights

Thu, 07 May 2026 00:00:00 +0000

Secondary T-cell lymphoma arising from pre-existing clones in a patient with diffuse large B-cell lymphoma during epcoritamab treatment following CAR-T therapy

Wed, 24 Dec 2025 00:00:00 +0000

Cytotoxic T-cell lymphoma with muscle involvement and germline variants in inborn error of immunity-related genes: clinical and genetic insights from a case series

Chong Wei, Danqing Zhao, Congwei Jia, Kaini Shen, Wei Zhang, Daobin Zhou — Thu, 04 Jun 2026 00:00:00 +0000

Sustained molecular clearance of the MYD88 p.L265P-mutant clone preceding resolution of cold agglutinin syndrome after autologous stem cell transplantation

Thu, 04 Jun 2026 00:00:00 +0000

Luspatercept in myelodysplastic syndrome with ring sideroblasts: a case report of intrapulmonary vascular dilatation syndrome causing protracted inexplicable hypoxia

Ayesha Warsi, Marie E. Faughnan, Rena Buckstein — Thu, 11 Jun 2026 00:00:00 +0000

Stuck in traffic: a bispecific antibody-mediated immune re-engagement after allogeneic stem cell transplantation

Stephanie Boisclair, Monica Wallin, Sally Ko, Douglas E. Gladstone — Thu, 14 May 2026 00:00:00 +0000

Lorlatinib-induced remission in refractory acute myeloid leukemia with an anaplastic lymphoma kinase fusion

Thu, 28 May 2026 00:00:00 +0000

On closing the gap: anti-PD-1-based salvage in relapsed/ refractory classical Hodgkin lymphoma. Comment on: “Mind the gap: anti-PD-1 salvage before autologous transplantation in classical Hodgkin lymphoma”

Hishan Tharmaseelan, Bastian von Tresckow — Thu, 28 May 2026 00:00:00 +0000

The gap narrows but shifts. Response to Comment on: “Mind the gap: anti–PD-1 salvage before autologous transplantation in classical Hodgkin lymphoma”

Daniel Noerenberg — Thu, 04 Jun 2026 00:00:00 +0000

Erratum to: “Extracellular vesicles mediate the communication between multiple myeloma and bone marrow microenvironment in a NOTCH dependent way”

Sun, 01 Nov 2026 00:00:00 +0000

Erratum to: “Cyp7b1-inhibiting azoles enhance hematopoietic stem and progenitor cell mobilization in normal and sickle cell disease mice”

Sun, 01 Nov 2026 00:00:00 +0000