bims-hemali Biomed News
on Hematologic malignancies
Issue of 2026–06–14
27 papers selected by
Alexandros Alexandropoulos, Γενικό Νοσοκομείο Αθηνών Λαϊκό



  1. Hemasphere. 2026 Jun;10(6): e70386
      Follicular lymphoma (FL) is the most common indolent lymphoma. Although chemoimmunotherapy is effective, toxicity remains problematic, and novel treatments are required. We performed a Phase Ib/II study of obinutuzumab, lenalidomide, and venetoclax in patients with treatment-naïve, high tumor burden, advanced-stage FL. During induction (6 × 28-day cycles), patients received obinutuzumab and venetoclax (in four dose levels from 400 mg day [D]1-10 to 800 mg daily) from Cycles 1 to 6 and lenalidomide (20 mg Days 1-21) from Cycles 2 to 6. Patients with complete response (CR) received 2 years maintenance obinutuzumab, while partial responders received 2 years obinutuzumab plus 6 months of venetoclax and lenalidomide. Genomic characterization and measurable residual disease (MRD) monitoring were performed using targeted next-generation sequencing (NGS) by circulating tumor DNA (ctDNA). Fifty patients were enrolled with a median age 60. No maximum tolerated dose was defined, and the Phase II dose of venetoclax was 800 mg daily. The CR rate and objective response rate were 86% and 92%, respectively. At median follow-up of 18.3 months, the 2-year progression-free survival and overall survival rates were 92% and 100%, respectively. The most common any-grade adverse events were neutropenia (72%), diarrhea (52%), and upper respiratory infection (48%). Undetectable MRD after one cycle of therapy had a 95% negative predictive value for relapse, while detectable MRD after three cycles of therapy had a 75% positive predictive value. Obinutuzumab, lenalidomide, and venetoclax are active in patients with treatment-naïve high tumor burden FL; however, myelosuppression impacted deliverability. ctDNA MRD is a promising biomarker in FL.
    DOI:  https://doi.org/10.1002/hem3.70386
  2. Blood Adv. 2026 Jun 10. pii: bloodadvances.2026019764. [Epub ahead of print]
      In the phase 3 STARGLO trial (NCT04408638), glofitamab plus gemcitabine-oxaliplatin (Glofit-GemOx) demonstrated superior overall survival (OS) vs rituximab (R)-GemOx, in patients with autologous stem cell transplant (ASCT)-ineligible relapsed/refractory (R/R) diffuse large B-cell lymphoma (DLBCL). We present efficacy and safety from STARGLO, with 3 years of follow-up, including in clinically relevant subgroups. After a median OS follow-up of 35.1 months (data cut-off: May 1, 2025), Glofit-GemOx continued to demonstrate favorable outcomes vs R-GemOx, respectively: median OS, 25.5 vs 12.5 months (hazard ratio [HR], 0.60; 95% confidence interval [CI], 0.4-0.8); median progression-free survival (PFS), 14.4 vs 3.3 months (HR, 0.41; 95% CI, 0.3-0.6); complete response (CR) rate, 58.5% vs 25.3%. Glofit-GemOx was particularly efficacious in the second-line (2L) vs third-line plus setting (3-year OS rate [95% CI]: 54.6% [45.2-64.0] vs 33.2% [21.2-45.3]). In 2L patients with primary refractory disease or early treatment failure the 36-month OS rate was 46.1% (95% CI, 35.2-56.9) with Glofit-GemOx vs 16.5% (95% CI, 3.4-29.6) with R-GemOx. Glofit-GemOx was favorable over R-GemOx regardless of patient age, with consistent efficacy observed across age categories, including in elderly patients (aged ≥75 years). No new safety signals were identified. With extended follow-up, fixed-duration Glofit-GemOx continues to demonstrate superior survival vs R-GemOx in ASCT-ineligible patients with R/R DLBCL, with favorable outcomes pronounced in the 2L setting, and consistent across subgroups including elderly and early relapsing patients. These data support Glofit-GemOx as an effective off-the-shelf treatment with curative potential in R/R DLBCL.
    DOI:  https://doi.org/10.1182/bloodadvances.2026019764
  3. Blood Adv. 2026 Jun 11. pii: bloodadvances.2026019701. [Epub ahead of print]
      Among patients with chronic myeloid leukemia (CML) aiming for tyrosine kinase inhibitor (TKI) discontinuation, second-generation TKIs (2G-TKIs) are used as one of the first-line options because they induce faster and deeper molecular responses than imatinib. However, predictors of attaining and sustaining MR4.5 (BCR::ABL1 International Scale [IS] ≤ 0.0032%) during 2G-TKI therapy remain undefined. We analyzed 431 patients enrolled in the phase III Japan Adult Leukemia Study Group (JALSG) CML212 trial, comparing nilotinib at 300 mg twice daily (n = 218) and dasatinib at 100 mg once daily (n = 213) as first-line therapy. The objective was to identify predictors of MR4.5 attainment and TKI discontinuation eligibility (TDE). Candidate variables assessed within 6 months included the EUTOS long-term survival (ELTS) score; BCR::ABL1 IS at baseline, 3 months, and 6 months; and IS-derived halving times, HT(0-3) and HT(3-6). TDE was defined as ≥3 years of TKI therapy with ≥2 consecutive years of sustained MR4.5. With a median follow-up of 3.0 years, the cumulative incidence of MR4.5 was 46.6%, and 36.3% of patients achieving MR4.5 met TDE criteria. In multivariable models, HT(0-3) (subdistribution hazard ratio [HR], 2.23; 95% CI, 1.09-4.55) and the 6-month IS (HR, 0.38; 95% CI, 0.31-0.47) were independent predictors of MR4.5 attainment, whereas only the 6-month IS predicted TDE (odds ratio, 0.37; 95% CI, 0.24-0.56). This study demonstrates that molecular response at 6 months after TKI initiation has important clinical value in early stratification of MR4.5 attainment and TDE in patients receiving 2G-TKI therapy.
    DOI:  https://doi.org/10.1182/bloodadvances.2026019701
  4. Ann Hematol. 2026 Jun 12.
      Central nervous system multiple myeloma (CNS-MM) is a rare yet highly aggressive plasma cell dyscrasia with a poor prognosis. CNS-MM represents a distinct clinical entity characterized by unique diagnostic challenges and therapeutic resistances. Conventional therapies have historically yielded dismal outcomes, with median survival measured in months. Modern diagnosis relies on integrating neurological symptoms, advanced CSF flow cytometry, and high-resolution imaging; however, unified diagnostic criteria remain lacking. In the modern era, multimodal strategies incorporating radiotherapy, BBB-penetrating agents, and immunotherapy have expanded treatment options. Bispecific antibodies and CAR-T therapy demonstrate unprecedented CNS-specific response rates, although data remain limited. This review synthesizes current evidence on CNS-MM epidemiology, risk factors, diagnostics, and therapeutics, highlighting emerging immunotherapeutic approaches and persistent knowledge gaps.
    Keywords:  Bispecific Antibodies; Blood-Brain Barrier (BBB); CAR-T Therapy; Central Nervous System Multiple Myeloma (CNS-MM)
    DOI:  https://doi.org/10.1007/s00277-026-07114-w
  5. J Clin Oncol. 2026 Jun 11. 101200JCO2601159
       PURPOSE: Revumenib is an oral inhibitor of menin-KMT2A, a key dependency in acute myeloid leukemia (AML) with KMT2A rearrangement (KMT2Ar), NPM1 mutation (NPM1mt), or NUP98 rearrangement (NUP98r). Preclinical studies suggest synergy with BCL2 inhibition.
    PATIENTS AND METHODS: In this phase 1-2 study, we evaluated an all-oral regimen of revumenib, decitabine/cedazuridine, and venetoclax in patients ≥12 years of age with relapsed or refractory AML. Decitabine/cedazuridine was given days 1-5, venetoclax days 1-14, and revumenib twice daily days 1-28. The primary objectives were to determine the recommended phase 2 dose (RP2D) and to assess efficacy according to the composite complete remission (CRc) rate.
    RESULTS: Forty-two patients were enrolled (median age, 40 years; range, 12-82) including 40% with KMT2Ar, 38% with NPM1mt, and 21% with NUP98r. Patients had a median of 2 prior lines of therapy; 52% had prior venetoclax. The RP2D of revumenib was 160 mg twice daily with a strong CYP3A4 inhibitor.Grade ≥3 adverse events included febrile neutropenia (36%), lung infection (21%), and thrombocytopenia (21%). Differentiation syndrome occurred in 10% (5% grade 3) and resolved with glucocorticoids.The CRc rate was 71%, and the CR or complete remission with partial hematologic recovery (CR/CRh) rate was 60%, with measurable residual disease negativity by flow cytometry in 80% of these patients. The median duration of CR/CRh for all patients was 10.5 months, not reached in KMT2Ar, 10.7 months in NPM1mt, and 5.9 months in NUP98r. Emergent mutations in the menin-binding site occurred in 13%.
    CONCLUSION: This combination was associated with high response rates and durable remissions, with an acceptable safety, in heavily pretreated patients with AML harboring alterations susceptible to menin inhibition.
    Keywords:  AML; KMT2A; NPM1; NUP98; menin
    DOI:  https://doi.org/10.1200/JCO-26-01159
  6. Adv Ther. 2026 Jun 11.
       INTRODUCTION: Zanubrutinib, acalabrutinib, and ibrutinib each demonstrated improved investigator-assessed progression-free survival (PFS-INV) and overall survival (OS) versus chemotherapy-based regimens in treatment-naive chronic lymphocytic leukemia (CLL) in the phase 3 trials SEQUOIA (NCT03336333), ELEVATE-TN (NCT02475681), and RESONATE-2 (NCT01722487), respectively. In the absence of head-to-head studies, this analysis compared the efficacy of zanubrutinib vs ibrutinib and vs acalabrutinib in treatment-naive CLL via indirect naive comparisons.
    METHODS: Eligibility criteria were aligned to improve cross-trial comparability. The zanubrutinib vs ibrutinib comparison included COVID-19-adjusted PFS-INV and OS in arm A of SEQUOIA (n = 241; median follow-up, 73.4 months) and the ibrutinib arm of RESONATE-2 (n = 136; median follow-up, 88.5 months). The zanubrutinib vs acalabrutinib comparison included PFS-INV and OS in subgroups of patients without del(17p) and/or TP53 mutations from arm A of SEQUOIA (n = 215; median follow-up, 73.6 months) and the acalabrutinib arm of ELEVATE-TN (n = 156; median follow-up, 74.5 months).
    RESULTS: Baseline characteristics were similar for each comparison. Zanubrutinib significantly prolonged PFS-INV (hazard ratio [HR], 0.65; 95% CI, 0.44-0.97; P = 0.0330) and showed a trend toward improved OS (HR, 0.60; 95% CI, 0.36-1.01; P = 0.0532) vs ibrutinib. At the 72-month landmark, PFS-INV and OS rates were significantly higher with zanubrutinib vs ibrutinib, with a risk difference of 15.3% (95% CI, 8.3-22.2%) for PFS and 9.9% (95% CI, 3.0-16.7%) for OS. Compared with acalabrutinib, zanubrutinib trended toward improved PFS-INV (HR, 0.76; 95% CI, 0.52-1.11; P = 0.1553) and OS (HR, 0.66; 95% CI, 0.41-1.06; P = 0.0836). The 72-month landmark PFS-INV and OS rates were significantly higher with zanubrutinib vs acalabrutinib, with a risk difference of 9.9% (95% CI, 3.0-16.9%) for PFS-INV and 8.8% (95% CI, 2.0-15.5%) for OS.
    CONCLUSION: These findings inform the long-term comparative efficacy of Bruton tyrosine kinase inhibitors and suggest that zanubrutinib may confer sustained PFS and OS benefits compared with ibrutinib and acalabrutinib in similar treatment-naive CLL populations. Graphical abstract and video available for this article. Overview of the Comparative Efficacy of Covalent BTK Inhibitors in Treatment-Naïve CLL/SLL With Six-Year Follow-Up (MP4 345006 kb).
    Keywords:  Acalabrutinib; BTK inhibitors; Covalent BTK inhibitors; Ibrutinib; Indirect treatment comparison; Treatment-naive chronic lymphocytic leukemia; Zanubrutinib
    DOI:  https://doi.org/10.1007/s12325-026-03661-w
  7. Med. 2026 Jun 12. pii: S2666-6340(26)00180-7. [Epub ahead of print]7(6): 101177
      Emerging therapies in multiple myeloma are challenging the long-standing paradigm of continuous disease control and raising the possibility of durable remission. Five pivotal clinical trials are evaluating transformative strategies, including replacement of transplantation, MRD-guided treatment, finite therapy, multi-target immune redirection, and early interception. Together, these studies may establish biology-driven, immune-based treatment frameworks aimed at achieving treatment-free remission and, ultimately, cure.
    DOI:  https://doi.org/10.1016/j.medj.2026.101177
  8. J Hematol Oncol. 2026 Jun 07. pii: 40. [Epub ahead of print]19(1):
      Although covalent and non-covalent Bruton tyrosine kinase inhibitors (BTKi) have extended clinical benefit to relapsed/refractory (R/R) and BTKi-resistant chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), there remains an unmet need for additional B-cell receptor (BCR) pathway targeted therapies for highly refractory disease. This summary highlighted latest updates from the American Society of Hematology 2025 Annual Meeting on emerging BTK-directed agents in CLL/SLL, including next-generation non-covalent BTKi, dual-kinase inhibitors, and BTK degraders. Phase 1 studies of docirbrutinib and rocbrutinib demonstrated target engagement across wild-type and resistance-associated BTK mutations with encouraging safety profiles and preliminary efficacy signals in heavily pretreated populations. Birletinib, a dual LYN/BTK inhibitor, showed a high objective response rate in patients with prior exposure to BTKi, BCL-2 inhibitors, and BTK degraders. BTK degraders, including bexobrutideg and BGB-16673, demonstrated rapid and deep responses, activity in high-risk molecular subgroups, and manageable toxicity profiles, with recommended phase 2 doses established. Collectively, these latest updates support continued clinical development of novel agents to address resistance and disease progression in R/R CLL/SLL.
    DOI:  https://doi.org/10.1186/s13045-026-01810-w
  9. Lancet Haematol. 2026 Jun 12. pii: S2352-3026(26)00112-2. [Epub ahead of print]
       BACKGROUND: Anthracycline-free regimens are needed for older adults with newly diagnosed diffuse large B-cell lymphoma (DLBCL). We aim to evaluate the efficacy and safety of fixed-duration epcoritamab monotherapy versus epcoritamab with lenalidomide in this patient population.
    METHODS: This open-label, multicentre, randomised, phase 2 trial was conducted at 44 hospitals across 11 countries in Europe and Asia. Patients had newly diagnosed, histologically confirmed CD20-positive large B-cell lymphoma, were ineligible for anthracycline-based chemoimmunotherapy (age ≥80 or ≥75 years with clinically significant comorbidities), had Ann Arbor stage II-IV disease, and an Eastern Cooperative Oncology Group (ECOG) performance status of 0-2. In stage 1, patients were randomly assigned (1:1) to epcoritamab monotherapy or epcoritamab with lenalidomide using a validated interactive response technology system and stratified by the International Prognostic Index (<3 vs ≥3) and ECOG performance status (0-1 vs 2). Epcoritamab was administered subcutaneously using a two step-up dosing schedule (0·16 mg on cycle 1 day 1 and 0·8 mg on cycle 1 day 8), followed by full 48 mg doses once per week in 28-day cycles during cycles 1-3 and once every 4 weeks during cycles 4-12 for up to 12 cycles. Lenalidomide (10 or 20 mg) was given orally once a day on days 1-21 of 28-day cycles for up to 12 cycles. Based on stage 1, one of the treatment regimens was selected for expansion in stage 2. The primary endpoint was investigator-assessed complete response rate (as of the data cutoff on Dec 5, 2025; Lugano criteria) in the full analysis set (all randomly assigned patients in stage 1 and in all treated patients in stage 2). Safety was analysed in patients who received ≥1 dose of trial treatment. This study is registered with ClinicalTrials.gov, NCT05660967 (active, not recruiting).
    FINDINGS: Between March 8, 2023, and May 14, 2025, 111 patients were assessed for eligibility (88 in stage 1 and 23 in stage 2) and 108 were treated. Median age was 83·0 years (IQR 80·0-86·0). 51 (47%) of 108 were male, 57 (53%) were female, and 87 (81%) were White. In stage 1, 44 patients each were randomly assigned to epcoritamab monotherapy or epcoritamab with lenalidomide and two did not receive treatment. At data cutoff, the complete response rate in stage 1 was 63·6% (95% CI 47·8-77·6; in 28 of 44 patients) in the epcoritamab monotherapy group and 45·5% (30·4-61·2; in 20 of 44) in the epcoritamab with lenalidomide group. The most common treatment-emergent adverse events (grade ≥3) were infections (eight [18%] of 44 patients) and fatigue (six [14%]) with epcoritamab monotherapy versus neutropenia (17 [40%] of 42) and infections (16 [38%]) with epcoritamab with lenalidomide; with serious adverse events in 28 (64%) versus 34 (81%). Treatment-emergent deaths occurred in six (14%) patients in the monotherapy group (cytomegalovirus infection reactivation, COVID-19 pneumonia, SARS-COV-2 infection, tumour lysis syndrome, neuroendocrine tumour of the lung, tumour haemorrhage) and six (14%) in the combined group (pneumonia, COVID-19 pneumonia, sepsis, general physical health deterioration, multiple organ dysfunction syndrome, acute cardiac failure). Based on differences in complete response rates and safety, epcoritamab monotherapy was selected for stage 2 and one patient did not receive treatment. In the epcoritamab monotherapy group, the complete response rate was 45·5% (24·4-67·8; in ten of 22) in stage 2 and 57·6% (44·8-69·7; in 38 of 66) across stages 1 and 2. The most common treatment-emergent adverse events (grade ≥3) among all patients who received epcoritamab monotherapy were infections (16 [24%]), neutropenia (eight [12%]), and hypertension (seven [11%]); with serious adverse events in 46 (70%). Treatment-emergent deaths occurred in two (3%) patients in stage 2 (multiple organ dysfunction syndrome and acute respiratory failure).
    INTERPRETATION: Fixed-duration epcoritamab monotherapy showed promising complete response rates and a manageable safety profile in older adults with newly diagnosed DLBCL and comorbidities, with slight differences between stages 1 and 2. Continued investigation of epcoritamab as a first-line chemotherapy-free treatment option is warranted.
    FUNDING: Genmab and AbbVie.
    DOI:  https://doi.org/10.1016/S2352-3026(26)00112-2
  10. Int J Clin Oncol. 2026 Jun 12.
      Despite recent progress in improving patient survival, the outcomes in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL) remain poor. For many years, R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) has been the standard first-line treatment for DLBCL; however, pola-R-CHP (polatuzumab vedotin, rituximab, cyclophosphamide, doxorubicin, and prednisone) has recently emerged as a new treatment option. In parallel, novel molecularly targeted therapies that target signaling pathways, cellular antigens, and epigenetic regulators associated with high-risk DLBCL are in development. Treatment strategies tailored to the cell of origin or to specific molecular subtypes are also being explored using subtype-specific targeted agents. In addition, agents that have demonstrated efficacy in patients with relapsed or refractory DLBCL-such as the anti-CD19 antibody tafasitamab and immunomodulatory drugs such as golcadomide-are currently under investigation for use in newly diagnosed patients. Immunotherapies, including anti-CD19-chimeric antigen receptor-T therapy and CD20×CD3 bispecific antibodies (BsAbs), have significantly improved outcomes in patients with relapsed or refractory disease and are now under evaluation as early-line therapies. BsAbs can enable more flexible treatment strategies, including combination regimens with cytotoxic or chemotherapy-free approaches. This review summarizes recent advances and ongoing trials that are investigating novel therapeutic strategies for newly diagnosed DLBCL that may soon be incorporated into clinical practice.
    Keywords:  Bispecific antibody; CAR-T; Cell of origin; Diffuse large B-cell lymphoma; Molecular subtype
    DOI:  https://doi.org/10.1007/s10147-026-03062-7
  11. J Clin Oncol. 2026 Jun 11. JCO2600947
       PURPOSE: In large B-cell lymphoma (LBCL), use of high-dose methotrexate (HD-MTX) to prevent CNS relapse (so-called CNS prophylaxis) remains controversial. International guidelines continue to recommend HD-MTX in patients deemed ultra high risk (UHR) because of a lack of robust data specific to these subgroups. This study was designed to examine the impact of HD-MTX specifically in UHR patients.
    METHODS: Data from two previous retrospective analyses were combined to produce a cohort of UHR patients (≥1 of the following criteria: CNS international prognostic index score 5-6; testicular, renal/adrenal, or breast involvement; ≥3 extranodal sites), treated with or without HD-MTX. The primary outcome was CNS relapse rate (isolated or concurrent with systemic relapse) measured from diagnosis with additional landmark analysis of all responding patients with no progression event at 6 months.
    RESULTS: Analyses were performed on 1,923 patients meeting UHR criteria. No significant difference in 3-year CNS relapse rate was observed between no HD-MTX (n = 1,051) versus HD-MTX patients (n = 872), including in multivariable analyses adjusting for baseline characteristics (3-year rate, 9.3% v 8.1%; adjusted hazard ratio [HR], 1.13 [95% CI, 0.82 to 1.57]). Analyses restricted to isolated CNS relapse also confirmed no difference (5.9% v 5.7%; adjusted HR, 1.03 [95% CI, 0.69 to 1.53]). In the landmark analysis (no HD-MTX n = 782, HD-MTX n = 773), no difference in 3-year CNS relapse was observed (6.7% v 6.6%, adjusted HR, 0.95 [95% CI, 0.62 to 1.44]).
    CONCLUSION: To our knowledge, this is the largest international comparative data set of patients with LBCL with UHR features showing no significant reduction in CNS relapse with HD-MTX in all UHR or in any individual subgroup. Despite inherent limitations of retrospective analyses, the data strongly support previous studies in suggesting HD-MTX prophylaxis has no meaningful benefit for most patients.
    DOI:  https://doi.org/10.1200/JCO-26-00947
  12. bioRxiv. 2026 Jun 03. pii: 2026.05.31.729063. [Epub ahead of print]
      The JAK2 V617F (JAK2 VF ) driver mutation is found in 95% of patients with polycythemia vera (PV), a progressive myeloproliferative neoplasm. Current treatments suppress excessive hematopoiesis but lack specificity for targeting JAK2 VF cells, are unable to deplete mutant stem/progenitor cells and ultimately result in drug resistance. We discovered that the FDA-approved antibiotic, linezolid (LZD), ameliorates the PV phenotype across multiple model systems. LZD suppressed cell proliferation and STAT5 signaling, altered the cell cycle, and increased apoptosis of JAK2 VF -harboring human erythroleukemia cells, but not in wild-type acute leukemia cells. Computational modelling indicated that LZD interacts specifically with mutant JAK2 VF but not with wild-type JAK2 protein. We further showed that, in JAK2 VF mice that faithfully recapitulate human PV, LZD mitigates disease burden by selectively targeting JAK2 VF stem cells thereby normalizing spleen size and blood counts. LZD also inhibited hematopoietic colony formation by patient-derived peripheral blood mononuclear cells, with the more primitive progenitors being preferred targets. Importantly, LZD selectively decreased JAK2 VF+ colony numbers, without impacting wild-type JAK2 colonies. In all, the data provide a firm foundation for evaluating LZD-like molecules as an effective therapy for PV and other myeloproliferative neoplasms.
    Key points: Linezolid acts as a JAK2 V617F IZselective inhibitor in PV mouse models and PV patient samples while sparing wildIZtype hematopoiesis. Linezolid acts directly on JAK2 V617F hematopoietic stem cells.
    DOI:  https://doi.org/10.64898/2026.05.31.729063
  13. Blood Adv. 2026 Jun 11. pii: bloodadvances.2026020255. [Epub ahead of print]
      Ruxolitinib is widely used in Polycythemia Vera (PV) following hydroxyurea failure. However, validated response criteria to predict long-term outcomes in ruxolitinib-treated patients are lacking, complicating clinical decision-making. We investigated predictors of event-free survival (EFS, including progression to post-PV myelofibrosis, thrombosis, hemorrhages, or death) after 6 months of ruxolitinib in 178 PV patients enrolled in the observational PV-ARC study (NCT06134102). After a median follow-up from ruxolitinib start of 3.50 years, 15 patients died, 7 had a thrombosis, 9 a hemorrhage, and 21 progressed to myelofibrosis. Overall, 5-year EFS was 70.4%. Leukocytosis (>10x109/L), thrombocytosis (>400x109/L), phlebotomy need, lack of spleen length reduction ≥50% (SR50) and ruxolitinib dose <10 mg BID at three timepoints (baseline, month 3 and 6), were tested for association with EFS. Multivariable analysis identified three independent risk factors: (1) ruxolitinib dose<10mg BID at ≥1 timepoint (HR 1.94, p=0.047), (2) no SR50 at months 3 and 6 (HR 2.65, p=0.009), (3) phlebotomy requirement at ≥2 timepoints (HR 2.11, p=0.039). Points were assigned as follows: 1 to phlebotomies at one timepoint; 2 to phlebotomies at ≥2 timepoints and to ruxolitinib <10 mg BID at ≥1 timepoint; 2.5 to lack of SR50. Based on cumulative scores, we developed the PV-Response to Ruxolitinib after 6 Months (PV-RR6) prognostic model, identifying three risk categories: low (score 0, 5-year EFS: 89.4%, n=63), intermediate (score 1-2.5, EFS: 71.0%, n=82), and high (score >2.5, EFS: 38.9%, n=33) (p<0.001). PV-RR6 enables early identification of patients at risk of poor outcomes, supporting timely treatment optimization in ruxolitinib-treated patients.
    DOI:  https://doi.org/10.1182/bloodadvances.2026020255
  14. Oncology. 2026 Jun 12. 1-19
      The standard induction regimen for newly diagnosed acute myeloid leukemia (AML) in eligible patients remains cytarabine-daunorubicin (7+3), although FLAG-based regimens are increasingly used in high-risk disease. We performed a PRISMA 2020-compliant systematic review and meta-analysis comparing FLAG-based induction with standard 7+3 in adults with newly diagnosed AML. Five retrospective cohort studies, including 534 patients, were analyzed. FLAG-based induction was associated with a significantly higher overall response rate than 7+3 (OR 1.83, 95% CI 1.03-3.22), without a significant difference in 30-day mortality (OR 0.56, 95% CI 0.12-2.69) or 60-day mortality (OR 0.79, 95% CI 0.29-2.14). Survival outcomes were heterogeneous and could not be pooled: median OS was similar in one cohort, whereas two studies reported improved OS with FLAG-based induction; DFS/RFS outcomes were inconsistently reported. FLAG-based induction was associated with higher receipt of consolidation therapy, while bridging to allogeneic transplantation did not differ significantly. Cytogenetic and molecular risk data were variably defined and incompletely reported, precluding reliable pooled subgroup analyses. Overall, FLAG-based induction improves response rates without a clear increase in early mortality or selected reported safety outcomes; however, its impact on survival remains uncertain and appears influenced by post-remission strategies. Prospective randomized trials are needed to better define its role in frontline AML therapy.
    DOI:  https://doi.org/10.1159/000552987
  15. Am J Hematol. 2026 Jun 07.
      
    Keywords:  curative; induction; intensive chemotherapy; randomized; venetoclax
    DOI:  https://doi.org/10.1002/ajh.70389
  16. Br J Haematol. 2026 Jun 10.
      Targeted therapies have transformed modern management of chronic lymphocytic leukaemia (CLL). Still, CLL remains an incurable disease, and key unresolved challenges include development of treatment resistance and intolerance. To address these challenges, it is necessary to define clinically actionable biomarkers that can predict individual treatment responses. Here, we aimed to map the treatment sensitivity and resistance landscapes of CLL cells from treatment-naïve and treatment-exposed patients to understand the evolution of treatment vulnerabilities. We performed ex vivo drug screens with 94 single agents and 87 drug combinations on CLL cells from treatment-naïve, ibrutinib-exposed or idelalisib-exposed patients. We found that overall drug sensitivity was reduced in cells from patients who had received treatment. Specifically, sensitivity to B-cell lymphoma 2 (Bcl-2) inhibitors was significantly reduced in both ibrutinib-exposed and idelalisib-exposed patient cells. Furthermore, combined Bruton's tyrosine kinase inhibitor (BTK)/Bcl-2 inhibition became less relevant in advanced disease, while dual mitogen-activated protein kinase kinase (MEK)/Bcl-2 inhibition was identified as an effective new treatment modality. Our findings provide valuable insights that may assist clinical decisions regarding treatment sequencing and treatment options for relapsed/refractory disease.
    Keywords:  BTK inhibitor; Bcl‐2 inhibitor; chronic lymphocytic leukaemia; drug sensitivity; targeted therapy
    DOI:  https://doi.org/10.1111/bjh.70603
  17. Nutrients. 2026 Jun 04. pii: 1807. [Epub ahead of print]18(11):
      Background/Objectives: Autoimmune gastritis (AIG), celiac disease (CD), and gastric surgery (GS) often cause iron deficiency anemia (IDA) due to iron malabsorption. In this clinical context, IDA treatment is often challenging. The first-line IDA treatment is oral iron supplementation followed by intravenous (IV) iron administration when ineffective or not tolerated. Ferric carboxymaltose (FCM) showed efficacy in various clinical settings. Prospective data evaluating the efficacy of IV FCM in IDA patients secondary to iron malabsorption are scant. The aim of the current study was to assess the tolerability, efficacy, and QoL impact of IV FCM for the treatment of IDA patients with iron malabsorption. Methods: Study design: single-center, prospective observational study: n = 37 adults with AIG, CD, or GS with IDA receiving IV FCM were consecutively included. Endpoints were (i) safety tolerability, (ii) efficacy on IDA recovery (Hb normalization), and (iii) QoL impact. At baseline (T0) and 12 weeks after treatment (T12), a QoL-SF12 questionnaire was assessed. Complete blood count (CBC) and iron status (ferritin, iron, transferrin, transferrin saturation (TS)) were assessed at T0, 4 weeks (T4), and T12 after treatment. Results: Of the 37 IDA patients, 19 (51.4%) had AIG, 9 (24.3%) CD, and 9 (24.3%) GS; Based on Ganzoni's formula, 24 (64.9%) patients received a single IV FCM infusion (mean ± SEM dosage of 975 ± 12 mg); 13 (35.1%) required two IV infusion sessions with a mean ± SEM cumulative dose of 1400 ± 77 mg. One patient (2.7%) experienced mild adverse events without need for treatment interruption or hospitalization. At T0, anemia was moderate in 7 (18.9%) patients and severe in 1 (2.7%). IDA recovery was achieved in 26 (70.3%) patients at T4 and in 29 (78.4%) at T12. At T4, mean ± SEM Hb increased from 10.8 ± 0.2 g/dL to 12.7 ± 0.1 g/dL, ferritin from 28.5 ± 11.2 ng/mL to 188.2 ± 25.7 ng/mL, and TS from 6.7 ± 0.5% to 23.7 ± 1.9% (p < 0.0001). At T12, mean ± SEM Hb further increased to 13.1 ± 0.2 g/dL (p < 0.05 vs. T4), ferritin slightly decreased to 125 ± 26.7 ng/mL, and TS to 22.7 ± 2.8%. At T12, nonsignificant increases in QoL scores relative to baseline were observed. Conclusions: IV FCM is a safe and effective treatment leading to IDA recovery in nearly 80% of patients at T12. Thus, when oral iron treatment is not feasible or has failed, IV FCM treatment might be considered a first-line therapeutic option for IDA consequent to iron malabsorption.
    Keywords:  autoimmune gastritis; celiac disease; ferric carboxymaltose; gastrointestinal iron malabsorption; intravenous iron therapy; iron deficiency anemia
    DOI:  https://doi.org/10.3390/nu18111807
  18. EJHaem. 2026 Apr;7(2): e70267
       Introduction: Marginal zone lymphoma (MZL) is an indolent yet incurable B-cell malignancy in which targeted agents such as BTK and PI3K inhibitors frequently fail due to resistance or toxicity. Antimicrobial peptides (AMPs), evolutionarily conserved effectors of innate immunity, possess selective cytotoxicity against malignant cells by exploiting tumor-specific membrane alterations.
    Methods: Peptides were synthesized and tested for their anti-proliferative activity in MZL cell lines.
    Results: We evaluated the antitumor activity of seven natural AMPs, including Antarctic fish-derived trematocines and chionodracine variants, and amphibian temporins, against MZL cell lines (VL51, Karpas1718) and derivatives resistant to BTK, PI3Kδ, or PI3Kα/δ inhibitors. Among them, W-trematocine and temporin L demonstrated potent dose-dependent cytotoxicity with IC50 values of 5.7-10 µM, maintaining full activity in all resistant models. Other peptides showed moderate activity, while chionodracine-1 was inactive. Notably, W-trematocine displayed minimal toxicity toward nonmalignant cells in prior studies, underscoring its selectivity. AMP-mediated killing, driven by membrane disruption and non-apoptotic death pathways, bypassed conventional resistance mechanisms, suggesting therapeutic potential in relapsed/refractory disease.
    Conclusion: Our findings highlight natural AMPs as promising candidates for development in drug-resistant MZL, warranting further optimization and preclinical validation.
    Keywords:  BTK; chionodracines; lymphoma; peptides; resistance; temporins; trematocines
    DOI:  https://doi.org/10.1002/jha2.70267
  19. Ann Med Surg (Lond). 2026 Jun;88(6): 3022-3023
      Multiple myeloma is a malignancy of clonal plasma cells characterized by progressive bone marrow infiltration, commonly presenting with anemia, bone pain, hypercalcemia, and renal dysfunction. T-cell bispecific antibodies (TCBs) have emerged as an effective therapeutic option in relapsed and refractory multiple myeloma, with G-coupled protein receptor, family C, group 5, member D (GPRC5D) representing a promising target due to its high expression in myeloma cells and limited presence in normal tissues. Forimtamig is a next-generation GPRC5D-targeting TCB with a novel 2:1 binding format - bivalently engaging GPRC5D and monovalently binding CD3ε on T cells. This structural advantage enhances avidity, stabilizes immunological synapses, and enables potent T-cell activation and cytotoxicity, even against low-antigen-expressing cells in immunosuppressive bone marrow environments. Preclinical studies show that forimtamig outperforms earlier 1 + 1 TCB formats by 50-200-fold in cell-killing efficiency. When combined with standard agents such as daratumumab, pomalidomide, or cereblon E3 ligase modulatory drugs, forimtamig has shown improved tumor clearance and reduced relapse rates. Its design also minimizes tumor escape by targeting the N-terminal region of GPRC5D. Currently undergoing phase 1 trials, forimtamig is being evaluated both as monotherapy and in combination regimens. Its high potency, favorable safety, and durable immune engagement make it a promising candidate in the evolving treatment landscape of multiple myeloma.
    Keywords:  GPRC5D-targeting TCB; Multiple myeloma; N-terminal region; forimtamig
    DOI:  https://doi.org/10.1097/MS9.0000000000004952
  20. EJHaem. 2026 Jun;7(3): e70311
       Introduction: Hairy cell leukemia (HCL) is an uncommon hematopoietic stem cell disease known to have an underlying somatic BRAFV600E driver mutation. Currently, the most accepted treatment is five or seven consecutive days of outpatient infusion of cladribine (e.g., continuous infusion), despite frequent antibiotic use and hospitalization with this regimen. As a result, a few investigators have adopted weekly infusion of cladribine with similar or improved results and fewer side effects.
    Methods: We conducted a retrospective, single-institution cohort study of 36 treatment-naïve patients with HCL treated at the University of Colorado Hospital. Eighteen patients received intermittent weekly cladribine (intermittent cladribine [IC]) for 5-7 doses and 18 received standard daily cladribine (continuous cladribine [CC]) over 5-7 days. We report clinical cohort characteristics, response rates, progression-free survival, overall survival, toxicity, hospitalization rates, and measurable residual disease monitoring in select patients using peripheral blood quantitative BRAFV600E PCR.
    Results: We report here our experience with 18 patients with newly diagnosed BRAF-mutated HCL treated with weekly cladribine at a single institution compared to 18 HCL patients who received continuous infusions. Baseline hematologic parameters and overall survival were comparable between groups (p = 0.1135), but there was a higher rate of complete remission for patients treated with IC (94.4% vs. 61.1%) with significantly improved progression-free survival (p < 0.0001). We observed comparable rates of neutropenia, neutropenic fever, antibiotic use, and G-CSF administration. There were fewer hospitalizations for patients treated with IC (4/18) compared to patients treated with CC (6/18). Rituximab exposure differed between groups, with 72% of patients in the IC cohort receiving rituximab compared with 27.2% in the CC cohort (although treatment status was documented for only 66.7% of patients in the CC cohort). Peripheral blood BRAFV600E allele burden significantly declined and correlated with clinical remission, but this was only performed in select patients who were treated in recent years.
    Conclusions: In this retrospective analysis, IC dosed weekly was associated with improved progression-free survival and higher rates of complete remission compared to CC with comparable toxicity and fewer hospitalizations. These findings suggest a potential clinical benefit from this regimen. However, interpretation of these findings is limited by the non-randomized design and differences in rituximab exposure between groups, which may have contributed to the observed outcomes and limited definitive conclusions.
    Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission.
    Keywords:  BRAF; cladribine; hairy cell leukemia
    DOI:  https://doi.org/10.1002/jha2.70311