Haematologica

Whole genome sequencing in acute myeloid leukemia

Torsten Haferlach — 2026-06-01

IGF2BP3 inhibition: another home run for RNA-binding protein targeting in hematological malignancies

Luiz O.F. Penalva — 2026-02-05

Don’t forget about thrombosis in acute promyelocytic leukemia

Martin S. Tallman — 2026-01-15

Would you, could you drive CARs to point-of-care manufacturing? Yes, you should!

Kim G. Hankey — 2026-01-29

Heart starts suffering early in sickle cell disease

Thomas d’Humières — 2026-02-12

The best laid schemes...

Mark J. Levis — 2025-11-27

Curing acute promyelocytic leukemia: no boost from immunity needed

Martin S. Tallman — 2025-11-06

Impact of insertion/deletion mutations affecting the ABL1 gene in Ph-positive leukemias

Chantal Lucini — 2026-02-12

NEAT1: a multifaceted long non-coding RNA in multiple myeloma

Gabriele Benini — 2025-12-18

Multiple myeloma (MM) is a plasma cell dyscrasia sustained by the clonal proliferation of plasma cells within the bone marrow. MM is the second most common hematologic neoplasm and, despite the continuous effort to overcome this disease, it remains uncurable. Throughout the recent years, novel therapeutic targets have been investigated, leading to the development of novel treatments for MM patients. In the last 10 years, interest in the long non-coding RNA NEAT1 has grown significantly within the field of cancer, including MM. In this review we offer a panoramic view of the role of NEAT1 in MM, with a focus on its possible role as both a biomarker and therapeutic target.

Optimal management of elderly/old Ph⁺ acute lymphoblastic leukemia patients

Robin Foà — 2026-01-22

Today, Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL) is a curable disease. In real life, too many adult ALL patients are not adequately worked up at diagnosis and treated, and this occurs, in particular, in elderly/old individuals. Here, we present representative case descriptions to discuss how Ph+ ALL patients diagnosed in their seventh, eight and ninth decade of life can, through a timely, accurate and personalized administration of tyrosine kinase inhibitor (TKI), without systemic chemotherapy, experience long-lived responses, minimal residual disease negativity, and a good quality of life. In this scenario, stopping TKI administration can also be considered. This perspective article represents a proof of concept that, nowadays, even in elderly/old Ph+ ALL, the disease can be cured or kept under prolonged control if adequately managed.

QKI dysregulation induces extensive splicing changes in T-cell acute lymphoblastic leukemia

Bruno Palhais — 2026-01-15

Understanding the molecular mechanisms underlying T-cell acute lymphoblastic leukemia (T-ALL) is essential for developing more effective therapeutic strategies. Despite therapeutic advances, the role of RNA-binding proteins in the pathogenesis of T-ALL remains poorly understood. Here, we investigate the RNA-binding Quaking protein (QKI), identifying it as a key regulator of splicing with tumor-suppressive properties in T-ALL. Through the analysis of two independent pediatric T-ALL cohorts, we demonstrate that QKI expression is frequently reduced in T-ALL, particularly within the HOXA subtype, and this reduction correlates with poor overall and event-free survival. Using T-ALL cell lines, we show that QKI depletion induces widespread splicing alterations, with numerous events corroborated in patient samples. Transcriptome profiling indicates that QKI downregulation leads to broad changes in gene expression, notably affecting pathways related to cell cycle progression, cholesterol homeostasis, and epithelial-mesenchymal transition. Functional assays demonstrate that QKI overexpression in T-ALL cells significantly reduces cell proliferation, induces G0/G1 cell cycle arrest, and limits leukemia progression and dissemination, ultimately improving survival in xenograft models. Together, these findings provide compelling evidence that QKI functions as a regulator of RNA splicing with tumor-suppressive activity in T-ALL.

NKX2-1 regulates cell survival, maturation, and DNAdamage responses as a cofactor of RUNX1 in T-cell acute lymphoblastic leukemia

Linde van Aerschot — 2026-01-08

T-cell acute lymphoblastic leukemia (T-ALL) is characterized by ectopic expression of transcription factors, including NKX2- 1, which is over-expressed in 5% of patients. NKX2-1 is associated with a cortical immunophenotype and drives metabolic addiction to the serine/glycine synthesis pathway in T-ALL. However, there is still no complete picture of the role of NKX2- 1 in T-ALL pathogenesis. We characterized a CRISPR-Cas9 NKX2-1 knockout model of RPMI-8402, the only known T-ALL cell line expressing NKX2-1, and validated the obtained results in patient samples. NKX2-1 knockout caused a less mature immunophenotype and promoted cell cycle progression, in line with the direct transcriptional repression of CDK6 by NKX2-1 that we observed. Furthermore, NKX2-1 protected T-ALL cells from apoptosis and DNA damage. The NKX2-1 protein directly bound DNA repair factors, such as RPA1 and RPA2, and presence of NKX2-1 resulted in differential expression of gene sets related to the repair of DNA damage in RPMI-8402 cells and patient samples. Furthermore, NKX2-1 positive cells showed less induction of DNA damage and apoptosis upon treatment with etoposide, a chemotherapy agent that causes DNA damage that is clinically used to treat T-ALL. Mechanistically, our data supported the hypothesis that RUNX1 is an important co-factor for NKX2-1 transcriptional regulation in T-ALL cells, and that NKX2-1 modulated the composition of RUNX1 protein complexes. Notably, NKX2-1 expressing cells showed higher sensitivity towards RUNX1 inhibition, suggesting a co-operative role in regulating T-ALL cell survival. This work reveals a critical role of NKX2-1 in enhancing T-ALL cell survival by protecting against DNA damage and identifies RUNX1 as an important co-factor in T-ALL pathogenesis.

A small molecule inhibitor of RNA-binding protein IGF2BP3 shows anti-leukemic activity

Amit K. Jaiswal — 2025-11-27

The RNA-binding protein IGF2BP3 is an oncofetal protein over-expressed in B-cell acute lymphoblastic leukemia and is critical for leukemogenesis in experimental models. With cancer-specific expression, functional dispensability for normal development, and an unleveraged pro-oncogenic function in mRNA homeostasis, IGF2BP3 represents an excellent target. With no small molecule inhibitors of IGF2BP3 in clinical use, we aimed to identify new IGF2BP3 inhibitors using biochemical methods. A biochemical screen, followed by a cell-based counter screen led to the identification of compounds with protein-RNA interaction inhibition and leukemic cell growth-inhibitory activity. One of these compounds, designated I3IN-002, shows consistent cell growth-inhibitory activity, altered cell cycle, and increased apoptosis in multiple leukemia cell lines, and is the most potent inhibitor of IGF2BP3 reported to date. I3IN-002 was tolerated in mice when administered intraperitoneally and showed potent anti-leukemic activity in a syngeneic transplantation model of MLL-Af4 leukemia. I3IN-002 inhibits the function of IGF2BP3, disrupting in situ binding of IGF2BP3 to target mRNA, and altering IGF2BP3-dependent gene expression regulation. Furthermore, cell-free and cellular thermal shift assays, as well as drug affinity responsive target stability assays support on-target activity of I3IN-002 for IGF2BP3. Thus, the identification of I3IN-002 paves the way for the discovery of potent and selective small molecule inhibitors of IGF2BP3.

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

Elias Jabbour — 2026-01-08

Obecabtagene autoleucel (obe-cel) is a CD19-targeted autologous chimeric antigen receptor T-cell therapy (CAR T) with a fast off-rate binding domain, administered as split-dose infusions guided by pre-lymphodepletion tumor burden (low-tumor- burden [TB] group: ≤20%; high-TB group: >20% bone marrow [BM] blasts). Obe-cel treatment in adult relapsed/refractory B-cell acute lymphoblastic leukemia (R/R B-ALL) was investigated in the phase Ib/II FELIX trial. Here, we report pharmacokinetics, safety, and efficacy outcomes in patients with low or high tumor burden and discuss the evidence/rationale justifying the spilt-dose strategy and threshold used to classify the groups. Tumor burden at lymphodepletion was a critical driver of CAR T-cell expansion; a 50% increase, e.g., 70% versus 20% BM blasts, was associated with a 1.9-fold increase (95% confidence interval: 1.4-2.6) in maximal expansion of CAR T cells. Robust CAR T-cell expansion was observed in both tumor burden groups. The incidence of grade ≥3 cytokine release syndrome and immune effector cell-associated neurotoxicity syndrome was minimal in both the low- and high-TB groups (2% vs. 3% and 4% vs. 9%, respectively). Although the overall remission rate was higher in the low-TB group (85%), it also remained high in the high-TB group (73%). Evidence from FELIX suggests that use of tumor burden--guided dosing may mitigate the typical effects of immunotoxicity while maintaining substantial efficacy. Although further study is needed to better characterize the effects of the split-dosing strategy, the clinical evidence supports its use when administering obe-cel for the treatment of R/R B-ALL. Trial registered at www.clinicaltrial. gov (clinicaltrials gov. Identifier: NCT04404660).

A scoring system to predict life-threatening thromboischemic events in patients with acute promyelocytic leukemia: the PETHEMA/PALG study

Rebeca Rodríguez-Veiga — 2025-11-13

Acute promyelocytic leukemia (APL) is a highly curable leukemia characterized by life-threatening coagulopathy leading to hemorrhagic and thrombo-ischemic events. We analyzed the incidence, outcomes and risk factors of thrombo-ischemic events in a large series of 1,210 patients with newly diagnosed APL reported to the PETHEMA registry. Therapy consisted of ATRA and chemotherapy (AIDA-based). Median age of patients was 46 years (range 2-90 years). Fifty-eight patients (5%) did not start the AIDA regimen either because they were unfit for chemotherapy, or because of early death before initiating ATRA. A total of 195 (16%) patients developed thrombo-ischemic events, the most frequent being superficial-vein and/or central catheter-related (6.9%) followed by central nervous system (2.2%), deep-vein thrombosis (2.1%), pulmonary embolism (2.1%), acute myocardial infarction (1.6%), or other locations (1.2%). Thrombo-ischemic events mostly occurred at diagnosis and during induction (4.0% and 9.3%, respectively). Patients developing life-threatening thrombo-ischemic events (i.e., excluding superficial and/or catheter-related) at diagnosis / induction had a 31% early death rate. Prolonged activated partial thromboplastin time (aPTT), age >40 years, ECOG performance status >1, platelets >25x109/L, and absence of bleeding at presentation were independent risk factors for life-threatening thrombo-ischemic events. Using these variables (1 point each), we developed and validated the Thromb-On risk score, identifying a high-risk group (3-5 points). The Thromb-On risk score was validated in a cohort of 585 patients treated since 2017 with arsenic trioxide plus all-trans retinoic acid (ATRA) (<10x109 leukocytes) or according to the AIDA protocol (≥10x109 leukocytes). This study could help to improve prevention and management of life-threatening thrombo-ischemic events through risk-adapted guidance, potentially leading to a decrease in early mortality in APL.

Locally manufactured versus commercial CAR T therapy for large B-cell lymphoma: a multicenter propensity scorematched analysis

Ronit Marcus — 2025-12-24

Locally manufactured chimeric antigen receptor T-cell (CAR T) therapy enables rapid manufacturing and a substantially shorter vein-to-vein time. However, its clinical efficacy compared to commercial CAR T products remains unclear. This retrospective study compared outcomes in patients with large B-cell lymphoma (LBCL) treated with a CD19-directed autologous locally manufactured CAR T product (CD28-based co-stimulation) versus axicabtagene-ciloleucel (axi-cel) or tisagenlecleucel (tisa-cel) across three academic centers. All patients had received at least two prior lines of therapy. Propensity score analysis for CAR T product adjusted for age, Karnofsky performance status, lactate dehydrogenase (LDH) level, primary refractory disease, and transformed histology was performed to account for underlying differences in treatment groups. Among 330 patients (132 axi-cel, 104 tisa-cel, 94 locally manufactured products), those treated with locally manufactured CAR T were younger, had higher performance status, and were more likely to present with elevated LDH and primary refractory disease. The median time from apheresis to CAR T infusion was significantly shorter with locally manufactured CAR T (11 days) than with axi-cel (38 days) or tisa-cel (44 days) (P<0.001). In adjusted analysis, a trend to improved progression-free survival with axi-cel was found when comparing locally manufactured products versus axi-cel (weighted hazard ratio [WHR]=1.54; 95% confidence interval [95% CI]: 1.00-2.37; P=0.051) and no difference between those given a locally manufactured product versus tisa-cel (WHR=0.71; 95% CI: 0.45-1.11; P=0.13). Overall survival was comparable across treatment groups: locally manufactured product versus axi-cel (WHR=1.35, 95% CI: 0.87-2.10; P=0.18) and locally manufactured product versus tisa-cel (WHR=0.85, 95% CI: 0.53-1.34; P=0.48). Rates of grade ≥2 cytokine release syndrome were lower with locally manufactured CAR T. These findings support locally manufactured CAR T as a clinically comparable alternative to commercial products for LBCL, with the potential advantage of rapid availability for patients with aggressive disease.

Mmrn1 expression defines a novel subset of hematopoietic stem cells and leukemia stem cells with great self-renewal potential

Naicheng Chen — 2026-01-22

Hematopoietic stem cells (HSC) are critical for lifelong blood cell generation. After mutation accumulation and functional disruption, HSC may transform into leukemic stem cells (LSC), leading to malignant hematological disorders. However, both HSC and LSC are highly heterogeneous, which hinders our comprehensive understanding of their biological characteristics and clinical application. Here, we identified multimerin 1 (Mmrn1) as a reliable marker for the most primitive HSC and LSC. We found that Mmrn1 was abundantly present in human and mouse HSC. Interestingly, HSC with high levels of Mmrn1 displayed increased quiescence and regenerative capacity, accompanied by megakaryocytic lineage commitment. Importantly, Mmrn1 deficiency gradually impairs HSC self-renewal under stress of transplantation due to reduced quiescence. Additionally, we noticed that Mmrn1 was specifically upregulated in acute myeloid leukemia (AML) cells, and its overexpression predicted poor patient prognosis. Further investigation revealed that Mmrn1 marked a subset of quiescent LSC responsible for AML initiation and development, and that deletion of Mmrn1 delays AML progression. Collectively, these data broaden our knowledge of stem cell heterogeneity in the context of normal and malignant hematopoiesis and advance the precision diagnosis and therapy of AML in the clinic.

Ligature-induced periodontitis promotes Dnmt3a^R878H-driven clonal hematopoiesis

Qiao Yuan — 2026-01-22

Characterized by somatic mutations (e.g., DNMT3A) in blood cells, clonal hematopoiesis (CH) is an age-related process wherein mutated hematopoietic stem and progenitor cells (HSPC) expand. This expansion thereby increases the risk of allcause mortality, myeloid hematologic malignancies and other non-malignant disorders, yet the risk factors that contribute to CH are still largely unknown. Periodontitis induces low-grade systemic inflammation and affects an estimated 62% of dentate adults globally, which may influence CH-associated pathologies. Periodontitis was modeled by bilateral maxillary second-molar ligation in mice; CH was established using hematopoietic-specific Dnmt3a^R878H mutant mice. Periodontal bone destruction was assessed via micro-computed tomography and hematoxilin and eosin staining. Changes in bone marrow HSPC, peripheral blood cells, and gingival immune cells were analyzed by flow cytometry. Key molecular mediators were identified through transcriptomic sequencing of sorted gingival myeloid cells and serum cytokine arrays. Results showed that ligature-induced periodontitis (LIP) promoted Dnmt3a^R878H-driven clonal hematopoiesis, manifested as a myeloid-biased phenotype characterized by increased myeloid cells in the gingiva and peripheral blood. The selective enrichment of the Dnmt3a^R878H clones during LIP is primarily because Dnmt3a^R878H HSC exhibit enhanced resistance and maintain competitive advantages within inflammatory microenvironments. Transcriptomic analysis revealed upregulation of Ccl17 in gingival R878H myeloid cells, which was corroborated by elevated serum and bone marrow levels of CCL17. The CCL17 upregulation drove myeloid cells recruitment to the gingiva, exacerbating periodontitis while simultaneously reinforcing Dnmt3a^R878H HSC expansion. This study highlights the necessity of controlling local chronic inflammation, such as periodontitis, in the clinical management of CH.

Sequential therapy with allogeneic HCT in patients aged ≥70 years with active AML: a single-center retrospective analysis

Odelia Amit — 2026-01-22

Patients ≥70 years with relapsed/refractory acute myeloid leukemia (AML) have an extremely poor prognosis. We adopted a sequential therapy approach, aiming to proceed directly to allogeneic hematopoietic cell transplantation (HCT) despite active disease. We analyzed results of all consecutive patients aged over 70 years and diagnosed with primary refractory/ relapsed AML who underwent HCT with sequential therapy approach (FITCy regimen) in the Tel Aviv Sourasky Medical Center. Fifty-one patients (median age 72 years; primary refractory N=42; relapse N=9). Median follow-up was 35 (range, 12-91) months. Incidences of overall and grade 3-4 acute graft-versus-host disease (GVHD) were 39.2% (95% confidence interval [CI]: 25.6-52.8), and 5.9% (95% CI: 0.0-12.5), respectively. Incidences of overall and moderate-severe chronic GVHD were 40.0% (95% CI: 25.7-57.1) and 29.4% (95% CI: 13.2-46.9), respectively. Non-relapse mortality at 3 years was 36% (95% CI: 22- 49). Forty-two of 51 patients (82.4%) had CR on day +30 post HCT. Relapse incidence at 3 years was 27.8% (95% CI: 14.3-41.2). GVHD-free relapse-free and overall survival (OS) at 3-years were 30% (95% CI: 19-47) and 31% (95% CI: 17-55), respectively. Multivariable analysis showed that worse European LeukemiaNet 2022 score, relapsed AML (vs. primary-refractory), not receiving ATG, and lower albumin prior to conditioning, were associated with higher mortality. We developed a model to predict OS that showed median OS in the low-, intermediate-, and high-risk group, not reached, 32.9 months, and 2.1 months, respectively, P<0.001. We conclude that sequential therapy in elderly patients with active AML demonstrates a strong anti- leukemic effect, and age alone should not be a barrier to this strategy.

Isolated KRAS and NRAS mutations in adults with monocytosis and/or cytopenia(s)

Sa A. Wang — 2025-12-24

NRAS and KRAS mutations, commonly identified alongside ancestral co-mutations, are generally regarded as pathogenic in adults presenting with monocytosis and/or cytopenia(s). However, their significance in isolation is not well defined. We studied a multi-institutional cohort of 52 patients with isolated RAS mutations and found that 26 (50%) did not meet diagnostic criteria for a myeloid neoplasm. Compared to patients with typical chronic myelomonocytic leukemia/myelodysplastic syndrome, these patients exhibited distinctive clinical features, including a younger age (65 years; range, 29-92 years), female predominance (60%), frequent immune-related disorders (39%), and splenomegaly (65%). Mutations predominantly involved KRAS (92%), with 87% affecting codons G12 or G13, and typically occurred at high variant allele frequency (39.0%; range, 2.6-53.0%). In three flow-sorted samples, KRAS/NRAS mutations were detected not only in granulocytes and monocytes but also in lymphocytes, reminiscent of pediatric RASopathies. A subset of patients (7/26, 27%) progressed to develop a myeloid malignancy, with acquisition of additional genetic alterations or the development of dysplasia. These findings challenge the assumption that isolated RAS mutations are sufficient to diagnose myeloid neoplasms. Instead, some cases may reflect adult-onset RASopathies or early clonal proliferations with distinct biological behavior. Recognition of such cases warrants refinement of diagnostic criteria and may influence therapeutic decision-making.

Platelet recovery delay and survival in patients with myelofibrosis undergoing allogeneic hemopoietic stem cell transplantation

Federica Sora' — 2026-01-15

We studied platelet recovery in 93 patients with myelofibrosis, following an allogeneic hemopoietic stem cell transplant (HSCT). The primary end point of the study was achieving a platelet count of 50x109/L within day +100 post transplant, which occurred in 62 patients (67%), predicted 5-year non-relapse mortality (NRM) (5% vs. 55%, P=0.0009) and 5-year actuarial survival (85% vs. 38%, P<0.00001); relapse was unaffected. The cumulative incidence of strong platelet recovery was predicted by a matched sibling donor (MSD) compared to alternative donors (90% vs. 60%, P=0.001), by the dose of CD34+ cells (cut off 8.68x106/kg; 83% vs. 61%, P=0.01), recipient age (cut off 63 years; 72% vs. 48%, P=0.01), and splenectomy (86% vs. 63%, P=0.04). In multivariate Cox analysis, significant predictors of platelet recovery were a MSD (P=0.003), a high CD34 cell dose (P=0.02), splenectomy (P=0.003), and younger patient age (P=0.02). Patients with slow platelet recovery have significantly lower platelet counts long term, combined with chronic graft-versus-host disease. In conclusion, strong post-HSCT platelet recovery in MF patients is mainly predicted by donor type, together with CD34 cell dose and patient age, and is strongly associated with NRM and survival.

Improving the predictive value of end-of-treatment PET/ CT in diffuse large B-cell lymphoma

Anne L. Bes — 2026-01-08

The 5-point Deauville score (DS) assesses end-of-treatment (EOT) response on positron emission tomography-computed tomography (PET/CT) in diffuse large B-cell lymphoma patients, categorizing scans as ‘positive’ or ‘negative’ for complete metabolic response. However, the positive predictive value (PPV) is suboptimal at 60%. We evaluated whether quantitative PET parameters combined with clinical data could improve prediction of treatment failure in EOT PET-positive patients. Baseline and EOT PET/CT scans of 138 patients in DS groups 4-5 were analyzed. Lesions were segmented using a semi-automated adaptive method (SUV4.0 or MV3). PET parameters, including total metabolic tumor volume (TMTV), number of lesions (NOL), tumorSUV/liverSUV-ratio (TLR), the maximum distance between the largest and any other lesion (DmaxBulk), and changes over time, were obtained. Two Cox regression models predicted 2-year progression-free survival. Clinical data were combined with EOT PET in model 1, and baseline, EOT, and delta values in model 2. After internal bootstrapping, models were evaluated for classification using different risk-of-progression cutoffs. Sensitivity, specificity, PPV, and negative predictive values (NPV) were determined. Using forward selection, model 1 comprised two variables: the NOL and the tumorSUVpeak/liverSUVmean (TLRpeakmean) at EOT (AIC=690.072, c-index=0.747). Model 2 incorporated NOL, TLRpeakmean (EOT) and baseline SUVmean (AIC=687.064, c-index=0.762). The PPV improved to over 85% without compromising the NPV. False positives dropped from 54 (39%, by DS) to 9 (7%) and 6 (4%) for models 1 and 2, respectively. Adding baseline features did not notably impact the models’ performance. Our models could support more accurate response-adapted treatment decisions, reducing unnecessary subsequent false positive-directed treatments to just 7%.

Left ventricular strain and chamber dimensions in pediatric sickle cell disease: age-related reduction in myocardial deformation independent of hemolysis and hydroxyurea therapy

Ziad Bulbul — 2025-12-18

Sickle cell disease (SCD) is associated with cardiovascular complications. Speckle-tracking echocardiography enables early detection of myocardial dysfunction before abnormalities appear in conventional echocardiographic parameters. This study evaluated left ventricular (LV) global longitudinal strain (GLS) in pediatric SCD patients, and its relationship with traditional LV function indices, disease complications, markers of hemolysis, and disease-modifying therapy. We retrospectively analyzed 278 echocardiograms from 185 participants (118 SCD patients, mean age 12.2 years; 67 age- and sex-matched controls, mean age 11.8 years) obtained between 2015 and 2023. Among the SCD cohort, 66.1% had the HbSS genotype, 9.3% had HbSβ⁰-thalassemia, and 17.8% had HbSβ⁺-thalassemia; the majority (83.9%) were on hydroxyurea. Compared to controls, SCD patients had significantly lower, but still normal, GLS (–21.5% vs. –22.3%; P<0.001), along with significantly larger chamber diameters, elevated mitral valve E velocity, E/A ratio, and tricuspid regurgitation maximal velocity. Prior stroke (β=0.9) and avascular necrosis (β=1.51) were independently associated with worse GLS. Patients with the different genotypes did not exhibit significant differences in GLS. The strain values did not correlate with hemolysis markers, suggesting that other mechanisms may underlie myocardial impairment. A significant age-related decline in GLS was detected, with an inflection point at approximately 9.9 years. Longitudinal analysis of LV strain in the SCD cohort demonstrated a small decline from –21.6% to –21.2% over a 3.7-year follow-up period. Finally, pediatric SCD patients exhibit significant cardiac remodeling and diastolic dysfunction with preserved, yet lower, LV GLS, underscoring the need for further research in this population.

Accurate automated diagnosis of B-acute lymphoblastic leukemia using deep learning and flow cytometry

Sulov Chalise — 2026-01-08

Multicenter upfront randomized phase II trial of quizartinib and high-dose cytarabine plus mitoxantrone in relapsed/refractory acute myeloid leukemia with FMSlike tyrosine kinase 3 internal tandem duplication

Sonia Jaramillo — 2025-11-20

Telomere attrition is common in patients with germline RUNX1 pathogenic variants

Rialnat A. Lawal — 2026-01-08

Immune intervention is dispensable for retinoic acid/ arsenic therapy of murine acute promyelocytic leukemia

Cécile Esnault — 2025-09-11

Two episodes of Ph⁺ acute leukemia with divergent Ig/TCR rearrangements in two patients with persistent BCR::ABL1 positivity: a 17-year follow-up

Alba Rubio-San-Simón — 2025-12-24

Unexpected impact on immunohematological diagnostics from transplantation of autologous stem cell preparations containing daratumumab

Kathrin Luckner — 2025-12-18

Deletion mutations of the ABL1 gene in Philadelphia chromosome-positive acute lymphoblastic leukemia: high prevalence with limited clinical impact

Hirofumi Takano — 2025-11-20

Venetoclax with intensive induction chemotherapy in newly diagnosed adult acute myeloid leukemia: early outcomes from a real-world experience

Aakanksha Naik — 2025-12-24

Promoter hypermethylation as a reversible mechanism of resistance to GPRC5D-directed therapy in multiple myeloma

Seungbin Han — 2026-01-08

Impact of the plasma cell quantification method on the International Myeloma Working Group diagnostic criteria for MGUS/SMM

Atsushi Uehara — 2025-12-18

Attenuated antibody responses to respiratory syncytial virus vaccination in hematologic malignancies: impact of anti-CD20 therapy

Yair Herishanu — 2026-01-08

Clinical outcomes of venetoclax combined with hypomethylating agents versus hypomethylating agents alone in TP53-mutated myelodysplastic syndromes

Mahmood Aldapt — 2026-01-08

Single-cell dissection of plasma cell clonal evolution to smoldering multiple myeloma after CD19 CAR-T cell therapy in B-cell acute lymphoblastic leukemia

Heye Yu — 2026-02-12

Late-onset progressive multifocal leukoencephalopathy after teclistamab in multiple myeloma: extending the timeline of infectious risk

Davide Chizzoniti — 2026-02-19

Blinatumomab-induced remission of refractory immune thrombocytopenia in pediatric acute lymphoblastic leukemia: a case report

Yaning Ao — 2026-01-29

Erratum to: “Multilevel defects in the hematopoietic niche in essential thrombocythemia”

Ting Sun — 2026-06-01