bims-hemali Biomed News
on Hematologic malignancies
Issue of 2026–09–20
24 papers selected by
Alexandros Alexandropoulos, Γενικό Νοσοκομείο Αθηνών Λαϊκό



  1. Curr Hematol Malig Rep. 2026 Sep 18. pii: 21. [Epub ahead of print]21(1):
       PURPOSE OF REVIEW: Therapeutic goals in BCR::ABL1-negative myeloproliferative neoplasms (MPNs) are evolving to include biologically anchored measures of disease modification with control of blood counts, splenomegaly, and symptoms. Disease modification endpoints and their linkage to survival in MPNs were central to the framework of MPN Asia 2026, which took place in Seoul. This review summarizes key themes from MPN Asia 2026 and relevant recent literature, examining the evolving roles of molecular response and long-term clinical benefits within a broader disease-modification framework across polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF).
    RECENT FINDINGS: Clinical trials with ropeginterferon alfa-2b were central to the discussions given these studies have contributed to the evolving paradigm of disease modification in MPNs, underscoring the importance of molecular response and event-free survival (EFS) in MPN management. In PV, ropeginterferon alfa-2b treatment provides a clinical model linking durable hematologic control and deep JAK2V617F variant allele frequency (VAF) reduction with improved long-term outcomes such as EFS, and prospective treatment-discontinuation strategies. Data from Europe and Asia supports the importance of early disease control, adequate interferon exposure, and longitudinal molecular monitoring. In ET, randomized data with ropeginterferon alfa-2b and emerging new treatment approaches such as lysine-specific demethylase 1 inhibition and mutant CALR-directed therapy are incorporating molecular endpoints into clinical development. However, the association between VAF reduction and thrombosis prevention, disease modification, EFS, and treatment-free remission (TFR) need to be elucidated. In MF, molecular profiling is already integral to prognostication and treatment selection, and disease modification assessment will likely require endpoints encompassing more than symptoms and spleen response, such as anemia response, bone marrow fibrosis change, clonal evolution, patient-reported outcomes, and importantly progression-free and overall survival. Molecular response, clonal suppression, prevention of vascular and progression events, survival outcomes such as EFS and TFR play increasingly important roles in MPN management.
    Keywords:   CALR ; JAK2V617F; Disease modification; Essential thrombocythemia; Molecular response; Myelofibrosis; Myeloproliferative neoplasms; Polycythemia vera; Ropeginterferon alfa-2b
    DOI:  https://doi.org/10.1007/s11899-026-00790-5
  2. Mediterr J Hematol Infect Dis. 2026 ;18(1): e2026066
      
    Keywords:  Adverse events; Chronic-phase chronic myeloid leukemia; Flumatinib; Molecular response; Real-world study; Tyrosine kinase inhibitor
    DOI:  https://doi.org/10.4084/MJHID.2026.066
  3. Am J Hematol. 2026 Sep 15.
       DISEASE OVERVIEW: Hairy cell leukemia (HCL) and HCL-like disorders, including HCL variant (HCL-V) and splenic diffuse red pulp lymphoma (SDRPL), are a very heterogeneous group of mature lymphoid B-cell disorders characterized by the identification of hairy cells, a specific immunophenotypic and genetic profile, a different clinical course and the need for appropriate treatment.
    DIAGNOSIS: Diagnosis of HCL is based on morphological evidence of hairy cells, characteristic flow cytometric immunophenotype (CD11c, CD103, CD123, CD25) bone marrow trephine biopsy which makes it possible to specify the degree of tumoral bone marrow infiltration and presence of the Annexin A1 marker in immunohistochemistry, and presence of the BRAFV600E mutation.
    RISK STRATIFICATION: Progression of patients with HCL is based on a large splenomegaly, leukocytosis, a high number of hairy cells in the peripheral blood and the unmutated ImmunoGlobulin HeaVy (IGHV) chain variable region gene mutational status. VH4-34 positive HCL cases are associated with a poor prognosis, as well as the rare cases of HCL with TP53 mutations and HCL-V.
    TREATMENT: Patients should be treated only if HCL is symptomatic. Chemotherapy with purine analogs (PNAs) are indicated in first-line HCL patients. The use of chemo-immunotherapy combining cladribine (CDA) and rituximab (R) represents an increasingly used therapeutic approach. Management of relapsed/refractory disease is based on the use of BRAF inhibitors (BRAFi) plus R, MEK inhibitors (MEKi), Bruton Tyrosine Kinase inhibitors (BTKi) and/or Bcl-2 inhibitors (Bcl-2i). The optimal sequence of the different treatments remains to be determined.
    Keywords:  hairy cell leukemia (HCL); hairy cell leukemia like disorders; hairy cell leukemia variant (HCL‐V); splenic diffuse red pulp lymphoma (SDRPL)
    DOI:  https://doi.org/10.1002/ajh.70441
  4. Front Med (Lausanne). 2026 ;13 1788083
       Background: Philadelphia chromosome-positive mixed phenotype acute leukemia (Ph+ MPAL) is a rare and aggressive hematologic malignancy. The incorporation of tyrosine kinase inhibitors (TKIs) into acute lymphoblastic leukemia (ALL)-like regimens has improved survival for Ph+ MPAL. However, the benefit of ALL-like chemotherapy backbones for adult patients, particularly those with bilineal disease, appears limited and is often hampered by significant toxicity. To the best of our knowledge, this case adds to the limited clinical experience regarding the use of azacitidine, venetoclax, and dasatinib in Ph+ MPAL. Novel, safer strategies are urgently needed.
    Case presentation: A 32-year-old man presented with a one-week history of fever. Bone marrow examination revealed 83% blasts with two distinct populations: lymphoblasts and monoblasts, confirming bilineal B/myeloid MPAL. Karyotyping showed 45, XY,-7, t(9;22)(q34;q11.2), and the BCR::ABL (p190) fusion gene was positive. Molecular genetics identified an EVI1 fusion gene and an ASXL1 mutation. The patient received one cycle of induction therapy with azacitidine, venetoclax, and dasatinib, augmented with Vincristine, prednisone, and homoharringtonine. Complete remission was achieved following this cycle, with the primary adverse event being grade IV myelosuppression, managed without severe infection, tumor lysis syndrome or organ dysfunction. After three consolidation cycles, flow cytometry showed negative minimal residual disease (MRD); however, BCR::ABL1 remained detectable at 0.3289%. The patient subsequently underwent haploidentical hematopoietic stem cell transplantation (haplo-HSCT). At the most recent follow-up, BCR::ABL1 was undetectable.
    Conclusion: An induction regimen based on azacitidine, venetoclax, and dasatinib may represent a safe and effective therapeutic strategy for adult patients with Ph+, bilineal MPAL, particularly when augmented with agents targeting distinct lineage components.
    Keywords:  Ph+ MPAL; azacitidine; case report; dasatinib; venetoclax
    DOI:  https://doi.org/10.3389/fmed.2026.1788083
  5. Blood. 2026 Sep 18. pii: blood.2026033895. [Epub ahead of print]
      To describe the impact of adding a tyrosine kinase inhibitor (TKI) to intensive chemotherapy (IC) on the outcome of de novo BCR::ABL1+ acute myeloid leukemia (AML), we retrospectively analyzed the data of 212 adult AML with ≥20% bone marrow blasts, BCR::ABL1+ or t(9;22)(q34.1;q11.2), no history of previous chronic myeloid leukemia and no prior exposure to BCR-ABL1 TKI. Eighty-nine patients were treated with IC alone and 123 with IC+TKI between 1999 and 2024. Complete remission (CR) or CR with incomplete hematologic recovery (CRi) was achieved in 52/77 patients (68%) with IC and 110/123 patients (89%) with IC+TKI (P<0.0001). With a median follow-up of 66.7 months, the median overall survival (OS) was 20.5 months with IC and not reached with IC+TKI. The 3-year and 5-year OS rates were 42.1% and 38.5% with IC and 70.9% and 62.9% with IC+TKI (P<0.0001) respectively. In multivariate analyses, the addition of TKI to IC was significantly and independently associated with an improved CR/CRi rate (odds ratio: 4.74 [95% confidence interval: 2.17-10.35]; P<0.001) and OS (hazard ratio: 0.40 [0.27-0.62]; P<0.001). Also, adding TKI to IC and alloHSCT in CR1 were independent prognostic factors for relapse-free survival (HR: 0.42; 95% CI: 0.23-0.75; P=0.004 and HR: 0.31; 95% CI: 0.17-0.55; P<0.0001). The outcome of de novo BCR::ABL1+ AML is strongly improved by the addition of a TKI to IC and should become the standard of care. The classification as adverse-risk should be reconsidered in the future ELN classification.
    DOI:  https://doi.org/10.1182/blood.2026033895
  6. Expert Opin Pharmacother. 2026 Sep 15.
       INTRODUCTION: Waldenström macroglobulinemia (WM) is an indolent B-cell lymphoma with unique clinical manifestations driven by both tumor infiltration of the bone marrow and extramedullary tissues, as well as IgM-related pathology. Recent therapeutic advances for WM have been largely driven by molecular discoveries, and current agents have significantly improved disease control and progression-free survival. However, WM remains incurable, and novel treatment strategies that balance efficacy with tolerability are needed.
    AREAS COVERED: This review summarizes current treatment approaches, including chemoimmunotherapy and Bruton tyrosine kinase inhibitors, and discusses emerging therapeutic strategies with a focus on clinical efficacy, toxicity, and evolving treatment paradigms. We also examine the role of combination approaches and novel agents, considering their potential integration into the current treatment landscape.
    EXPERT OPINION: Despite substantial progress, key challenges remain, including the absence of definitive comparative data between various treatment strategies, the optimal sequencing of available agents, and an understanding of the impact of novel therapies on the depth of hematologic response, as well as long-term clinical and patient-reported outcomes. Future efforts should focus on biologically informed treatment selection and the development of strategies that reduce cumulative toxicities while achieving durable disease control.
    Keywords:  Bruton tyrosine kinase inhibitors; Chemoimmunotherapy; Waldenström macroglobulinemia; cellular therapies; targeted therapies
    DOI:  https://doi.org/10.1080/14656566.2026.2734125
  7. Am J Hematol. 2026 Sep 17.
      Patients with newly-diagnosed acute myeloid leukemia (ND-AML) derive variable survival benefit from venetoclax (Ven) plus hypomethylating agent (HMA) therapy, and the optimal Ven duration across genetic risk groups remains undefined. Among 540 ND-AML patients receiving Ven-HMA at Mayo Clinic, outcomes were compared across Ven 7- (n = 33), 14- (n = 117), 21- (n = 96), and 28-day (n = 294) schedules during Cycle 1 and stratified by ELN 2024 and Mayo genetic risk groups. At a median follow-up of 37.7 months, allogeneic stem cell transplant (ASCT) rates were similar across Ven duration groups (15%, 18%, 18%, and 20% for 7-, 14-, 21-, and 28-day; p = 0.86). Median transplant-censored survival was comparable across Ven durations (13.3, 11.9, 16.8, and 13.2 months for 7, 14, 21, 28 days, respectively; p = 0.65), with outcomes driven by ELN risk (6.3, 11.5, 18.3 months for high, intermediate, low; p < 0.01) and Mayo genetic risk (6.9, 17.8 months, not reached; p < 0.01). Survival was comparable across Ven durations within ELN intermediate/low-risk and all Mayo risk groups. Among ELN high-risk patients, 14-day Ven was associated with inferior transplant-censored survival compared to 21- and 28-day schedules (p < 0.01). Notably, 30- and 60-day mortality were higher with shorter Ven schedules (7-day: 9%/18%; 14-day: 7%/15%) versus 28-day (2%/6%), which likely reflects treatment selection bias. In ND-AML, no significant difference in transplant-censored survival was observed across the 7-, 14-, 21-, and 28-day Ven schedules; prognosis was determined primarily by Mayo and ELN 2024 genetic risk rather than by Ven duration. Prospective trials are needed to establish risk-adapted Ven dosing strategies.
    Keywords:  karyotype; mutations; remission; survival; venetoclax
    DOI:  https://doi.org/10.1002/ajh.70500
  8. Lancet Haematol. 2026 Sep 17. pii: S2352-3026(26)00193-6. [Epub ahead of print]
       BACKGROUND: Rilzabrutinib showed robust efficacy and favourable safety profile in patients with persistent or chronic immune thrombocytopenia in the double-blind period of the phase 3 LUNA3 trial. We report long-term activity and safety of rilzabrutinib in the LUNA3 open-label period.
    METHODS: LUNA3 was a multicentre, randomised, phase 3 trial that was done at 103 centres in 24 countries in adolescents and adults. In this study, adults aged 18 years or older with primary persistent or chronic immune thrombocytopenia with a previous response to intravenous or anti-D immunoglobulins or corticosteroids were enrolled during the double-blind period and were randomised 2:1 to receive either rilzabrutinib 400 mg twice daily orally or placebo. Patients entered the 28-week open-label period either after completing the 24-week double-blind period or after week 12 if they did not meet predefined response criteria, in which they received rilzabrutinib 400 mg twice daily orally. Endpoints of this open-label study were evaluated as secondary (stable platelet response over the double-blind and open-label periods [no two platelet counts, at least 4 weeks apart, <50 × 109 platelets per L, without an intervening count of ≥50 × 109 platelets per L, within 24 weeks of initial platelet response] and safety) and exploratory (proportion of patients who received either placebo or rilzabrutinib during the double-blind period and had a durable response during the open-label period [platelet counts ≥50 × 109 platelets per L for at least two-thirds of at least ten non-missing weekly platelet counts during the last 16 of 28 weeks of the open-label period without rescue therapy]; complete response [platelet count ≥100 × 109 platelets per L on two consecutive visits at least 5 days apart without bleeding or rescue immune thrombocytopenia therapy]; Immune Thrombocytopenic Purpura Patient Assessment Questionnaire physical fatigue score; and immune thrombocytopenic purpura bleeding scale score). Activity and safety analyses were done in patients exposed to rilzabrutinib during the double-blind and open-label periods according to the intention-to-treat principle. This trial is registered with ClinicalTrials.gov (NCT04562766) and the EU Clinical Trials Register (2023-509401-71); the adult part of the trial is complete.
    FINDINGS: Between April 16, 2021, and Oct 15, 2024, 180 patients of the 202 patients randomly assigned during the double-blind period entered the open-label period (115 who were randomly assigned to rilzabrutinib and 65 to placebo during the double-blind period; median age 48 years [IQR 33-61], 112 [62%] females and 68 [38%] males, and 113 [63%] White). 46 (23%) of 198 patients exposed to rilzabrutinib in the double-blind and open-label periods had stable platelet responses by the data cutoff date of Oct 15, 2024 (31 [23%] of 133 in the double-blind rilzabrutinib group and 15 [23%] of 65 in the double-blind placebo group). Treatment-related adverse events occurred in 46 (26%) of 180 patients, of which the most frequent were grade 1 or 2 diarrhoea (17 [9%] patients) and nausea (17 [9%]). Treatment-related grade 3 adverse events occurred in four (2%) patients (one had hypertension, one had petechiae, one had interstitial lung disease, and one had bronchopulmonary aspergillosis and cytomegalovirus viraemia). Serious treatment-related adverse events occurred in two (1%) patients (interstitial lung disease and bronchopulmonary aspergillosis along with cytomegalovirus viremia). No deaths occurred during the open-label period. 14 (22%) of 65 patients in the double-blind placebo group had a durable platelet response). Median follow-up was 196 days (IQR 89-197). Complete response was attained by 42 (23%) of 180 patients. Physical fatigue (maximum mean change from baseline of 11·7 [SD 27·4] across all patients) and bleeding scores (mean change from baseline of -0·13 [SD 0·19]) were sustained or improved.
    INTERPRETATION: Rilzabrutinib showed continued, stable, and sometimes improved platelet responses, including in patients who were initially non-responsive in the double-blind trial. Additionally, rilzabrutinib improved several disease aspects, including physical fatigue and bleeding, supporting its multi-immune modulation mechanism in immune thrombocytopenia, and had a favourable safety profile. The long-term extension period of LUNA3 will further characterise the long-term efficacy and safety of rilzabrutinib in patients with difficult-to-treat immune thrombocytopenia, and the ongoing LUNA4 trial (NCT07007962) will determine the efficacy of rilzabrutinib in earlier-line treatment and its potential to achieve sustained treatment-free response.
    FUNDING: Sanofi.
    TRANSLATIONS: For the German, French, Japanese, Spanish, Arabic and Italian translations of the abstract see Supplementary Materials section.
    DOI:  https://doi.org/10.1016/S2352-3026(26)00193-6
  9. Nat Med. 2026 Sep 11.
      Teclistamab, a B cell maturation antigen-targeting bispecific antibody, has demonstrated substantial activity in relapsed multiple myeloma (MM), particularly in earlier lines of therapy, and may have higher efficacy in high-risk smoldering MM (HR-SMM) with a more functional immune system. In the randomized phase 2 ImmunoPRISM trial, we compared fixed-duration teclistamab with lenalidomide-dexamethasone (Rd) in HR-SMM. After a six-patient safety run-in, patients were randomized 2:1 to teclistamab or Rd. The primary endpoint was complete response (CR) rate. As of 26 May 2026, 59 patients were treated-45 received teclistamab and 14 received Rd. Teclistamab treatment induced a CR in 77.8% patients versus 0% with Rd, and minimal residual disease negativity at 10-5 in 82.2% patients. At a median follow-up of 24.5 months, 2-year progression-free survival was 92% with teclistamab versus 49% with Rd. Overall, response rates, duration of response and time to progression (TTP) were significantly improved in teclistamab compared to Rd. Toxicities in the teclistamab arm included grades 1-2 cytokine release syndrome, no neurotoxicity and no increase in grade 3 infections compared to Rd (20% versus 21%). No deaths occurred in either arm. Teclistamab represents a highly active immune-interception strategy for HR-SMM. ClinicalTrials.gov registration: NCT05469893 .
    DOI:  https://doi.org/10.1038/s41591-026-04642-w
  10. EClinicalMedicine. 2026 Oct;100 104193
       Background: Hydroxyurea (HU) is the most commonly used cytoreductive treatment for patients with myeloproliferative neoplasms (MPN), but emerging data on pegylated interferon-alpha2 (pegIFNα) are encouraging. Optimal first-line treatment remains unclear.
    Methods: DALIAH was a randomised, open-label, parallel-group, phase 3 trial conducted at nine centres in Denmark comparing HU with pegIFNα in patients with newly diagnosed MPN. Adults (≥18 years) with newly diagnosed or cytoreductive treatment-naïve MPN (essential thrombocythaemia [ET], polycythaemia vera [PV], prefibrotic myelofibrosis [pre-PMF], or primary myelofibrosis [PMF]; according to 2008 World Health Organization [WHO] criteria) and evidence of active disease were eligible, regardless of risk score. Patients aged >60 years were randomised (1:1:1) to either HU, pegIFNα-2a, or pegIFNα-2b; patients aged ≤60 years were randomised (1:1) to either pegIFNα-2a or pegIFNα-2b. The primary endpoint was the proportion of molecular responders (MR; partial or complete) at 18, 36, and 60 months (intention-to-treat [ITT], HU vs pegIFNα). This trial was registered with ClinicalTrials.gov, NCT01387763.
    Findings: Between Feb 7, 2012, and July 6, 2015, 203 eligible participants were enrolled in the modified ITT population (HU n = 38 [19%], pegIFNα n = 165 [81%]). In the ITT analysis, MR proportions were similar between HU and pegIFNα at 18 months (19% vs 21%, p = 1·00), 36 months (19% vs 26%, p = 0·64), and 60 months (23% vs 24%, p = 1·00). In the per-protocol (PP) analysis, restricted to patients who remained on therapy, pegIFNα showed higher MR beyond 36 months (36 months: 23% vs 56%, p = 0·01; 60 months: 35% vs 67%, p = 0·03). At month 60, PegIFNα discontinuation was high (65% vs 37% HU, p = 0·0019). No significant difference in grade ≥3 adverse events was observed between groups (HU 58% vs pegIFNα 45%, p = 0·21). Adverse events occurring in ≥10% of patients differed between treatments: dyspepsia, pyrexia, and urinary tract infections were more common with HU, whereas fatigue, influenza-like illness, injection-site irritation, myalgia, and decreased white cell blood count were more frequent with pegIFNα. Anaemia and decreased neutrophil count were the most common haematological events in both groups. Treatment-related adverse events were reported in 77 patients (HU 27% vs pegIFNα 41%, p = 0·14) and led to permanent discontinuation in 13 patients (all pegIFNα).
    Interpretation: HU and pegIFNα display distinct response kinetics. Molecular response was similar in the ITT analysis, reflecting that non-response largely resulted from higher pegIFNα discontinuation rather than lack of efficacy. Among patients who tolerated therapy, pegIFNα achieved superior long-term molecular responses. Findings should be considered within the context of the significantly higher treatment discontinuation rate with pegIFNα than with HU. These findings suggest that pegIFNα may offer long-term molecular benefit in selected patients highlighting the need for biomarkers that predict response and long-term tolerability, preferably already at diagnosis.
    Funding: OUH-Region Sjaelland Faelles Forskningspulje, Region Sjællands Sundhedsvidenskabelige Forskningsfond (RSSF) 2018, Gangstedfonden, OUH Frie Forskningsmidler, Swedish Orphan, Fonden til Lægevidenskabens Fremme, Ellen og Aage Fausboells Helsefond af 1975, and Desirée og Niels Ydes Fond.
    Keywords:  Efficacy and safety; Hydroxyurea; Molecular response; Myeloproliferative neoplasms; Pegylated interferon alpha2; Randomised controlled trial
    DOI:  https://doi.org/10.1016/j.eclinm.2026.104193
  11. Blood Adv. 2026 Aug 24. pii: bloodadvances.2025015950. [Epub ahead of print]
       BACKGROUND: Iron deficiency is the most common micronutrient deficiency, and when untreated progresses to anemia. Existing guidance on the diagnostic criteria for iron deficiency is limited and not evidence based.
    OBJECTIVE: These evidence-based guidelines of the American Society of Hematology (ASH) are intended to support patients, clinicians, and other health care professionals in their decisions about the diagnosis of iron deficiency taking a global perspective in all settings.
    METHODS: ASH established a multi-disciplinary guideline panel that included one patient representative and was balanced to minimize potential bias from conflicts of interest. The University of Kansas Health System supported the guideline-development process, including performing systematic evidence reviews on the prevalence of iron deficiency across populations and studies to inform diagnostic thresholds up to July 2025. The panel prioritized clinical questions according to clinical impact and high-risk populations. The panel used the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach, including GRADE Evidence-to-Decision frameworks, to assess evidence and make recommendations, which were subsequently open for public comment.
    RESULTS: The panel agreed on 5 recommendations.
    CONCLUSIONS: Key recommendations of these guidelines include serum ferritin thresholds for specific populations with the goal to prioritize the diagnosis of iron deficiency, irrespective of the presence of anemia, remarks for considerations of other diagnostic thresholds, and guidance on the diagnosis of iron deficiency in persons with inflammation. Gaps in the literature and research priorities were also identified.
    DOI:  https://doi.org/10.1182/bloodadvances.2025015950
  12. Leukemia. 2026 Sep 14.
      CD38 is a transmembrane glycoprotein highly expressed in acute myeloid leukemia (AML) and T-cell acute lymphoblastic leukemia (T-ALL). XmAb18968 is a novel CD38-CD3 bi-specific T-cell engager with Fc domain modified to reduce non-selective activation of effector cells. In this phase 1 multicenter clinical trial, we evaluated the outcomes of XmAb18968 in adults with relapsed/refractory (RR) AML and T-ALL. Twenty-two patients with AML (n = 13) and T-ALL (n = 9) with a median age of 63 years (range 31-77) were enrolled. Prior lines of therapy (median 3, range 1-8) included venetoclax (77.3%), allogeneic HCT (22.7%), CD7 CAR-T cell therapy and daratumumab (11.1%). Grade ≥3 adverse events included anemia (14%), neutropenia (18%), and thrombocytopenia (14%). No grade ≥3 cytokine release syndrome or neurotoxicity was seen. Overall, 17 patients (AML = 11, ALL = 6) completed at least one cycle of therapy. Among 11 patients with RR-AML, one achieved partial remission (PR) and two achieved MRD negative complete remission (CR). In 6 patients with RR-T-ALL, 4 achieved meaningful improvement in disease burden with 1 clearance of MRD. Median OS was 8.5 months in AML and 8.7 months in T-ALL. XmAb18968 is safe and tolerable with encouraging preliminary efficacy, supporting further investigation of CD38 targeting therapies in this setting (NCT05038644).
    DOI:  https://doi.org/10.1038/s41375-026-03130-x
  13. J Natl Compr Canc Netw. 2026 Sep;pii: e267019. [Epub ahead of print]24(9):
      The treatment of early-stage Hodgkin lymphoma is one of oncology's great success stories. Numerous large randomized trials have tested and refined conventional chemotherapy regimens, optimized radiation therapy (RT) approaches, explored the integration of metabolic imaging such as PET/CT, and are now evaluating novel agents. What was once a fatal disease is now cured in almost all patients. Combined-modality therapy, typically involving a short course of chemotherapy followed by low-dose, highly conformal RT, has emerged as the most effective strategy for achieving durable remissions. Nonetheless, concerns about the long-term toxicities associated with RT have prompted investigations into chemotherapy-only regimens as a potential alternative to combined-modality therapy. To date, neither interim nor postchemotherapy PET/CT imaging has been able to identify patients who can safely omit consolidation RT without compromising efficacy, although additional studies are ongoing. Meanwhile, novel agents such as nivolumab and brentuximab vedotin have significantly advanced the treatment of advanced-stage disease and are now demonstrating promising activity in early-stage Hodgkin lymphoma. In parallel with advances in systemic therapy, radiation technologies have also progressed substantially. Techniques such as proton therapy, intensity-modulated RT, and image-guided RT dramatically reduce radiation exposure to healthy tissues compared with historical approaches, thereby improving the therapeutic ratio. Despite the high cure rates achieved today, clinical trials continue to explore novel and personalized approaches to achieve long-term remission without compromising quality of life.
    DOI:  https://doi.org/10.6004/jnccn.2026.7019
  14. Cytometry B Clin Cytom. 2026 Sep 14.
      Circulating tumor plasma cells (CTCs) at diagnosis are independent prognostic markers in newly diagnosed multiple myeloma (NDMM). Flow cytometry (FC) enables sensitive and cost-effective CTC quantification, but prognostic cut-offs vary across studies. The methodological approach used for quantification may affect the determination of the CTC percentage. In this study we compare head-to-head two FC techniques [single-platform FC versus Next Generation Flow (NGF)] to measure CTC levels in NDMM patients. Methodological differences between the two techniques can be found in sample processing (NGF includes fixation and permeabilization steps that are not required for CTC quantification by single-platform FC) and analytical sensitivity, which is higher for NGF than for single-platform FC. The percentage of CTCs was simultaneously assessed with both techniques in the peripheral blood (PB) of 34 patients enrolled in the REAL MM trial (NCT03829371) at screening. Single-platform FC detected CTCs in 29/34 patients (85.3%) patients, while NGF detected CTCs in 31/34 patients (91.2%), including 2 cases that were negative by single-platform FC. The CTC percentage measured using the NGF technique (median 0.0049%, range 0%-0.377%) was significantly lower than that obtained using single-platform FC (median 0.009%, range 0%-0.59%) (p < 0.0001). Indeed, quantifying CTCs with FC after fixation and permeabilization (comparably to NGF) led to results that were similar to NGF. In conclusion, NGF demonstrated higher sensitivity than single-platform FC to detect CTCs at diagnosis in MM patients. Employing standardized techniques like NGF may avoid variability across different laboratories and centers.
    Keywords:  circulating tumor cells; flow cytometry; multiple myeloma
    DOI:  https://doi.org/10.1002/cyto.b.70068
  15. Ann Hematol. 2026 Aug 04. pii: 415. [Epub ahead of print]105(10):
      The addition of venetoclax to hypomethylating agents (HMAs) is standard for older adults with newly diagnosed acute myeloid leukemia (AML). However, prolonged venetoclax (VEN) exposure can cause cytopenias and infections, raising questions about optimal duration. We conducted a single‑center retrospective study of 102 patients treated between 2018 and 2025 with azacitidine or decitabine plus VEN administered for 14 (n = 22), 21 (n = 48), or 28 (n = 32) days per 28‑day cycle. Baseline cytogenetic and molecular profiling, responses by 2022/2024 ELN criteria, measurable residual disease (MRD), cumulative incidence of relapse (CIR), disease‑free survival (DFS), and overall survival (OS) were analyzed using competing‑risks regression and Cox models. Median age was 68 years and patients received a median of 4 cycles. Composite remission (CR/CRi/CRh/MLFS) was 66.7%, with MRD negativity in 75.0% of responders. Remission and MRD negativity rates did not differ significantly across VEN‑duration cohorts. Median OS and DFS were 17.3 and 12.3 months, respectively, with no significant differences in OS, DFS, and CIR between 14‑, 21‑, and 28‑day cohorts. Grade ≥ 3 cytopenias and transfusion independence rates also did not differ significantly. In this cohort, shortening VEN exposure to 14 or 21 days did not show a significant difference in response, survival, relapse risk, and toxicity profiles relative to a 28‑day schedule in our cohort. These findings support further prospective evaluation of reduced VEN durations in this population.
    Keywords:  AML; Elderly; Hypomethylating agents; Survival outcomes; Treatment duration; Venetoclax
    DOI:  https://doi.org/10.1007/s00277-026-07219-2
  16. J Genet Eng Biotechnol. 2026 Sep;pii: S1687-157X(26)00113-7. [Epub ahead of print]24(3): 100769
      The KIT gene, known as proto-oncogene c-Kit, encodes a receptor tyrosine kinase and plays a crucial role in cellular processes through activation that initiates signal transduction pathways. The KIT protein includes five extracellular domains, a kinase domain, a transmembrane helix, and a juxta-membrane domain. The study investigated these domains in chronic myeloid leukemia (CML) patients, revealing insights that enhance clinical protocols for tyrosine kinase inhibitors used in targeted therapy for hematological malignancies. However, mutations in the kinase domain present challenges by impairing drug binding. In this exploratory investigation, mainly through PCR and Sanger sequencing techniques, 50 samples (30 patients and 20 controls) were utilized. A total of 27 mutations were identified. While the following mutations (G753C, G538C, A415T, and A404G) were the most frequent, (G814C, G858T, G876T, and G880A) were only found in control cohort. Interestingly, many unique mutations were detected in the Iraqi population, suggesting specific genetic polymorphisms. Furthermore, the data showed that younger patients had better responses to imatinib with fewer dangerous mutations, while middle-aged patients faced significant resistance, which correlated with weight gain and obesity. Elderly individuals displayed a higher mutation burden, necessitating multiple treatment changes. Despite limitations, this exploratory study stressed the importance of considering patients' genetic backgrounds and BMIs to improve therapeutic outcomes for CML patients.
    Keywords:  Chronic myeloid leukemia (CML); KIT gene; Mutations; Tyrosine kinase inhibitors (TKIs)
    DOI:  https://doi.org/10.1016/j.jgeb.2026.100769
  17. Front Oncol. 2026 ;16 1933274
       Background: Arsenic disulfide (As2S2) inhibits proliferation and induces apoptosis in diffuse large B-cell lymphoma (DLBCL) cells, its clinical application is constrained by toxicity. Metformin has also been reported to exert antitumor effects across various malignancies. This study investigated whether metformin potentiates the anti-lymphoma efficacy of As2S2 in DLBCL cells and evaluated associated alterations in apoptosis-related markers and Hedgehog signaling molecules.
    Methods: DLBCL cell lines (DB and SU-DHL-4) were treated with metformin and/or As2S2. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay, apoptosis was determined by Annexin V/propidium iodide (PI) flow cytometry, and drug interactions were analyzed using the Bliss independence model and CompuSyn software. The expression levels of BAX, BCL-2, SMO, GLI1, and GLI2 were analyzed by quantitative real-time PCR and Western blotting.
    Results: Both metformin and As2S2 inhibited DLBCL cell proliferation in a dose- and time-dependent manner. Combination treatment resulted in significantly greater growth inhibition in both cell lines compared with either monotherapy, with synergistic effects confirmed by both Bliss and CompuSyn analyses. Furthermore, the combination significantly increased apoptosis relative to single-agent treatments. At the molecular level, combined treatment was associated with a pro-apoptotic shift in the BAX/BCL-2 ratio and downregulation of Hedgehog pathway components, including SMO, GLI1, and GLI2, with more pronounced changes observed at the protein level.
    Conclusions: Metformin enhances the anti-proliferative and pro-apoptotic effects of As2S2 in DLBCL cells in vitro. These effects are associated with modulation of the BAX/BCL-2 axis and suppression of Hedgehog pathway-related molecules. Further studies are warranted to elucidate the underlying mechanisms and to evaluate efficacy and safety in vivo.
    Keywords:  apoptosis; arsenic disulfide; diffuse large B-cell lymphoma; hedgehog signaling; metformin
    DOI:  https://doi.org/10.3389/fonc.2026.1933274
  18. Ann Hematol. 2026 Jul 24. pii: 416. [Epub ahead of print]105(10):
      Acute myeloid leukemia (AML) remains a highly heterogeneous malignancy in which outcomes are particularly poor for patients classified as having high-risk disease. Traditionally, high-risk AML has been defined by adverse baseline genetic features, including complex cytogenetics, TP53 alterations, and mutations associated with secondary or therapy-related disease. However, this static, genetics-centered definition is increasingly insufficient in the modern therapeutic era. Emerging evidence supports a more dynamic and context-dependent model in which risk is shaped not only by molecular architecture but also by treatment intensity, patient fitness, measurable residual disease (MRD), and evolving resistance mechanisms. Advances in genomic profiling have refined risk stratification frameworks, including ELN 2022 for intensively treated patients and the ELN 2024 classification for those receiving less-intensive therapies. In parallel, MRD has emerged as a powerful biomarker that reclassifies patients during treatment, identifying those with persistent, therapy-resistant disease despite morphologic remission. Biologically, high-risk AML is driven by the interplay of clonal evolution, epigenetic plasticity, leukemic stem cell persistence, and protective microenvironmental and immune interactions, all of which contribute to relapse. Therapeutically, the landscape has expanded to include targeted agents, venetoclax-based combinations, and transplantation strategies, yet outcomes remain limited in key high-risk subsets, particularly TP53-mutated disease and post-venetoclax relapse. Accordingly, current strategies emphasize rational combination therapies, MRD-guided treatment adaptation, and approaches targeting both leukemic cells and their supportive niches. In 2026, high-risk AML is best understood as a dynamic, treatment-context-dependent state. Improving outcomes will require integration of precision diagnostics, biologically informed therapy, and adaptive strategies designed to anticipate and overcome resistance.
    Keywords:  Acute Myeloid Leukemia; High-Risk; Precision Diagnosis; Treatment
    DOI:  https://doi.org/10.1007/s00277-026-07142-6
  19. Expert Rev Hematol. 2026 Sep 15. 1-3
      
    Keywords:  Myelofibrosis; anemia; janus kinase inhibitors; pacritinib; thrombocytopenia
    DOI:  https://doi.org/10.1080/17474086.2026.2732995
  20. Br J Haematol. 2026 Sep 19.
      Hyperdiploidy (HRD) is the most common genetic subtype in multiple myeloma (MM) but with significant prognostic heterogeneity. In this integrated Single Nucleotide Polymorphism (SNP-array) and Fluorescence In Situ Hybridization (FISH) analysis of 694 newly diagnosed Chinese MM patients, a modal chromosome count >49 predicted superior overall survival (OS, p = 0.0062) and progression-free survival (PFS, p = 0.00037), outperforming other metrics. Gain of chromosome 3 was favourable for OS (p = 0.0024) and PFS (p = 0.00078). Notably, HRD improved OS in patients with isolated 1q21+ (p = 0.011) but not in those harbouring high-risk abnormalities (t(4;14), t(14;16), 17p- or 1p32-). The prognostic value of modal count was cytogenetic abnormality (CA)-dependent: in HRD without high-risk CAs, >49 conferred better OS (p = 0.01) and PFS (p = 0.001); in isolated 1q21+, a favourable trend was observed; but no discrimination in other high-risk CAs. Autologous haematopoietic stem cell transplantation (AHSCT) significantly improved OS (p = 0.014) and showed a PFS trend (p = 0.062) only in HRD patients without high-risk CAs and with >49 chromosomes. In conclusion, modal chromosome count >49 and chromosome 3 gain are robust favourable markers in HRD. HRD provides survival benefit in isolated 1q21+. FISH-based detection of trisomy 3 may offer a rapid, economical alternative for risk assessment of HRD. AHSCT benefit is restricted to low-risk HRD with higher ploidy.
    Keywords:  SNP array; autologous haematopoietic stem cell transplantation; cytogenetic abnormalities; hyperdiploidy; multiple myeloma
    DOI:  https://doi.org/10.1111/bjh.70817
  21. Eur J Haematol. 2026 Sep 18.
      Advances in the treatment of large B-cell lymphoma (LBCL) have expanded therapeutic options beyond conventional chemoimmunotherapy to include cellular and targeted therapies. There is growing interest in identifying subsets of LBCL that may benefit from these novel approaches based on histopathologic and molecular features. Molecular subclassification has identified an LBCL A53 phenotype characterized by TP53 alterations, a subgroup historically associated with poor outcomes following standard therapy. To better define progression-free and overall survival outcomes in TP53-altered LBCL in the contemporary treatment era, we conducted a multicenter cohort study evaluating responses to first-, second-, and third-line therapies. Our findings demonstrate that TP53-altered LBCL can be cured with first-line curative intent chemoimmunotherapy. In the second and third-line setting, outcomes did not significantly differ between different treatment approaches, though improved PFS was seen with CAR-T in the second line for double hit patients. This study represents the largest reported cohort of patients with TP53-altered LBCL and provides important insights into treatment outcomes across lines of therapy in the era of novel agents.
    Keywords:  TP53; large B‐cell lymphoma; next generation sequencing
    DOI:  https://doi.org/10.1111/ejh.70330