bims-hemali Biomed News
on Hematologic malignancies
Issue of 2026–03–01
twenty-two papers selected by
Alexandros Alexandropoulos, Γενικό Νοσοκομείο Αθηνών Λαϊκό



  1. Biomedicines. 2026 Feb 11. pii: 408. [Epub ahead of print]14(2):
      Chronic myeloid leukemia (CML) has undergone a significant shift over the past two decades, transitioning from a fatal malignancy to a chronic, highly manageable disease with near-normal life expectancy for most patients. This transformation has been driven by the development of BCR-ABL1-targeted tyrosine kinase inhibitors (TKIs), which have enabled durable disease control and deep molecular responses (DMRs) in the majority of patients with chronic-phase CML. As long-term survival outcomes have plateaued across available agents, contemporary management has shifted beyond disease suppression toward optimizing long-term safety, quality of life, and the achievement of treatment-free remission (TFR). This review summarizes current evidence on molecular monitoring strategies, the comparative efficacy and toxicity profiles of first-, second-, and third-generation TKIs, and emerging advances in response assessment. Patient-centered TKI selection is discussed in the context of cardiovascular risk, comorbidities, treatment tolerability, and survivorship goals, reflecting the growing emphasis on individualized therapy in chronic-phase CML. Molecular monitoring strategies are examined in parallel, highlighting the clinical importance of early and sustained DMRs in guiding therapeutic decisions and TFR eligibility. Although RT-qPCR remains the standard for molecular monitoring, emerging high-sensitivity techniques such as digital droplet PCR and next-generation sequencing provide complementary value by improving the detection of low-level residual disease, refining risk stratification, and enabling earlier identification of resistance. Emerging therapeutic strategies and advances in response assessment further highlight ongoing efforts to enhance the depth and durability of remission while minimizing long-term toxicity. These developments support a more precise, individualized, and outcome-driven approach to modern CML management.
    Keywords:  chronic myeloid leukemia; deep molecular response; molecular monitoring; treatment-free remission; tyrosine kinase inhibitors
    DOI:  https://doi.org/10.3390/biomedicines14020408
  2. Blood Adv. 2026 Feb 24. 10(4): 1381-1394
       ABSTRACT: This phase 2 study evaluated the efficacy and safety of combining acalabrutinib and lenalidomide with either rituximab (ALR) or obinutuzumab (ALO), with longitudinal minimal residual disease (MRD) monitoring in frontline MCL treatment. The primary objective was molecular complete response (CR) after 12 cycles of induction, defined by Lugano criteria, and undetectable MRD of <10-6 (uMRD6) by clonoSEQ. Secondary objectives included safety, responses, and survival. Exploratory objectives included tumor mutation profiles and cell-free DNA (cfDNA) by cancer personalized profiling by deep sequencing. Patients in uMRD6 molecular CR were eligible for discontinuation of acalabrutinib plus lenalidomide after 24 cycles; all patients received a minimum of 36 cycles of anti-CD20 antibody treatment. In the ALR cohort, grade 3/4 hematologic toxicities included neutropenia (38%), thrombocytopenia (4%), and anemia (4%). Nonhematologic toxicities included rash (42%), fatigue (4%), nausea (4%), and vomiting (4%). The overall response rate (ORR) was 100%, CR rate was 83%, and molecular CR rate was 67% after 12 cycles of induction, with best molecular CR at 83%. At a median follow-up of 53 months (range, 46-60), the 4-year overall survival (OS) and progression-free survival (PFS) for ALR were 91% and 76%, respectively. TP53 mutations were adversely associated with PFS (P = .026). For ALO, ORR, CR, and molecular CR were 90% after induction, and 2-year OS and PFS were both at 100%. Longitudinal cfDNA analysis in ALR revealed clonal evolution during response and progression. This safe and active regimen is feasible as a time-limited initial therapy for patients with MCL and warrants further evaluation in response-adapted strategy. This trial was registered at www.ClinicalTrials.gov as NCT03863184.
    DOI:  https://doi.org/10.1182/bloodadvances.2025017760
  3. Am J Hematol. 2026 Feb 27.
      It is an exciting era in leukemia owing to the development of novel targeted therapies and advances in genomics, pathophysiology, prognostication, and monitoring (e.g., highly sensitive measurable residual disease assays). Currently, most leukemias are effectively treated with immunotherapies (highly effective monoclonal antibodies targeting CD19 [blinatumomab], or CD22 [inotuzumab ozogamicin]), BCR::ABL1 tyrosine kinase inhibitors (TKIs; e.g., dasatinib, ponatinib), Bruton TKIs (e.g., ibrutinib, acalabrutinib), BCL-2 inhibitors (venetoclax), IDH1/2 inhibitors (ivosidenib, olutasidenib, and enasidenib), FLT3 inhibitors (e.g., midostaurin, quizartinib, and gilteritinib), menin inhibitors (revumenib, ziftomenib), and chimeric antigen receptor T-cell therapies. These novel agents and their judicious use in combination strategies have transformed the treatment landscape across all leukemias, significantly increased survival and quality of life for patients, and attenuated the need for intensive chemotherapy and hematopoietic stem cell transplantation. Leukemia subtypes, such as Philadelphia-positive acute lymphoblastic leukemia (incurable before 2000) and chronic lymphocytic leukemia (previously considered incurable) with historically dire prognoses were recently transformed to favorable leukemias with 5- and 10-year survival rates of 80+% and 90+%, respectively. The BCR::ABL1 TKIs resulted in normal life expectancy in chronic myeloid leukemia. Notable advances have also been made in AML with targeted therapies, although some subsets (older/unfit patients for intensive chemotherapy, complex karyotype, TP53-mutated, KMT2A-rearranged, and treated secondary AML) still have unfavorable outcomes. Herein, we provide a high-level overview of prominent clinical developments across all leukemias. In contemporary times, harnessing the benefits of novel targeted therapies and the evolving treatment landscape bolster the optimistic view that most, if not all, leukemias are curable.
    DOI:  https://doi.org/10.1002/ajh.70247
  4. Blood Adv. 2026 Feb 26. pii: bloodadvances.2025019273. [Epub ahead of print]
      Approximately 80% of patients with diffuse large B-cell lymphoma achieve a complete response following chemoimmunotherapy as defined by PET scan. However, not all patients who fail to achieve a metabolic complete response are destined to relapse. In a number of these patients, the PET scan is falsely positive (i.e., 20%-40% in several large series), particularly when the PET scan score is Deauville 4. Reflexively intervening with salvage systemic therapy or radiotherapy in these patients is potentially harmful. It appears that very sensitive measurements of circulating tumor DNA might be able to differentiate between patients who are unlikely to relapse and those with residual lymphoma. It is important to remember that lymphoma is not the only condition that can make a PET scan abnormal and to consider alternate diagnosis that should be managed differently.
    DOI:  https://doi.org/10.1182/bloodadvances.2025019273
  5. Haematologica. 2026 Feb 26.
      Venetoclax (ven)+azacitidine (aza) is the standard of care for newly-diagnosed acute myeloid leukemia (AML) patients who are not candidates for intensive chemotherapy (IC). Because prognostic factors for ven/aza and IC differ, an AML patient fit for IC may derive more benefit from ven/aza. We therefore designed a trial for younger, newly-diagnosed AML patients with non-favorable risk disease to receive ven/aza regardless of "fitness" for IC. We aimed to understand toxicity and efficacy in this population, and retrospectively compared outcomes to matched IC patients. Newly-diagnosed non-favorable risk patients ≤60 were enrolled and received ven, dose escalated to 600mg/dailyx28 days, with aza 75mg/m2x7 days on a 28-day cycle. Subjects were encouraged to move expeditiously to allogeneic stem cell transplant (ASCT) in first remission. Thirty-six subjects enrolled. Median age was 49 (22-59). Grade ≥3 neutropenia(42%), anemia(33%), thrombocytopenia(53%) and febrile neutropenia(36%) were common. The overall response rate (ORR) was 25/36 (69%) with 19 (53%) complete remissions; 68% of responders achieved MRD-negativity. Most subjects (53%) bridged to ASCT, and the majority of non-responders were successfully salvaged with IC. The median progressionfree- survival (PFS) and overall survival (OS) have not been reached (median follow-up 2.9 years). Compared to IC matched controls, the ORR, ASCT rate and PFS were significantly improved (69% vs 44% [p=0.0495], 53% vs 28% [p-0.0290] and not reached vs 60.8 months [p=0.007]). Hospital days, transfusions and infectious complications were significantly reduced for ven/aza subjects. Ven/aza is feasible for newly-diagnosed, younger, non-favorable risk AML patients, and appears at least as effective as IC.
    DOI:  https://doi.org/10.3324/haematol.2025.300374
  6. Blood Adv. 2026 Feb 27. pii: bloodadvances.2025017575. [Epub ahead of print]
      Novel treatments that can improve disease course of essential thrombocythemia (ET) are needed. In this phase 2 trial, participants with ET who required cytoreduction and had inadequate response to or were intolerant of ≥1 standard therapy received bomedemstat at a starting dose of 0.6 mg/kg per day, titrated to achieve a target platelet count (200-400×109/L). Primary end points were safety and response, defined as a platelet count ≤400×109/L without new thromboembolic events. Seventy-three participants received bomedemstat. At 24 weeks, 49 of 64 evaluable participants (77%) had a response. Durable reductions in platelet count (≤400×109/L for ≥12 weeks) were observed in 52 of 72 participants (72%). Durable reduction in white blood cell count (<10×109/L for ≥12 weeks) was observed in 61 of 72 participants (85%); of 10 participants with elevated white blood cell count at baseline, 9 had normal white blood cell count (<10×109/L) at week 24. Hemoglobin levels remained stable. After 24 weeks of treatment, a decrease in variant allele frequency of CALR, JAK2, or MPL was observed in 39 of 46 (85%) evaluable participants. By week 24, 2 of 73 participants (3%) had experienced ≥1 thrombotic event and 15 of 73 (21%) experienced ≥1 hemorrhagic event. During overall treatment period, grade 3 or 4 adverse events (AEs) occurred in 34 of 73 participants (47%). AEs led to temporary treatment interruption in 29 participants (40%) and permanent discontinuation in 11 (15%). No participants died due to AEs. Bomedemstat had clinically relevant activity and manageable safety in participants with ET. Registration: NCT04254978 (Study of Bomedemstat in Participants With Essential Thrombocythemia [IMG-7289-CTP-201/MK-3543-003]).
    DOI:  https://doi.org/10.1182/bloodadvances.2025017575
  7. Front Immunol. 2025 ;16 1728452
      Hairy cell leukemia (HCL) is an indolent leukemic B-cell malignancy that typically presents with pancytopenia and splenomegaly. Many patients achieve durable initial remissions with nucleoside analogs but ultimately relapse as leukemic cells acquire or exploit resistance mechanisms. Central to this resistance is the highly specialized leukemic microenvironment, particularly within bone marrow and splenic niches where hairy cells persist despite clearance of circulating disease. These protective niches provide CXCR4- and adhesion-dependent retention signals, cytokine support, and immune-evasion mechanisms that sustain leukemic survival, promote minimal residual disease, and ultimately drive relapse. In this Mini Review, we summarize how stromal interactions, extracellular-matrix remodeling, and disrupted immune surveillance reinforce therapeutic resistance in HCL, and how BCR and MAPK signaling interact with these circuits. Further, we highlight emerging strategies, including agents that disrupt chemotaxis, adhesion, and immune checkpoints, designed to dismantle microenvironmental support and improve the depth and durability of remission in HCL.
    Keywords:  BCR signaling; CXCL12–CXCR4; MAPK pathway; TNF-α; fibrosis; hairy cell leukemia; immune-evasion; leukemic microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2025.1728452
  8. Br J Hosp Med (Lond). 2026 Feb 09. 87(2): 50847
      Multiple myeloma is a haematological malignancy of plasma cells, typically characterised by a monoclonal immunoglobulin protein detectable in the blood. Myeloma requires treatment when it affects specific end-organs, including lytic bone disease. The accurate detection of bone disease is therefore crucial in the diagnosis and management of myeloma, and advanced imaging with whole-body magnetic resonance imaging or positron emission tomography is now recommended as the standard of care. For patients with non-secretory myeloma and those with extramedullary disease, imaging is the only way to monitor response to treatment and to detect relapse. Whilst there are challenges in delivering advanced imaging modalities to patients with myeloma, the clinical and financial advantages mean that improving access should be a priority. This review discusses the importance of advanced imaging in the management of myeloma across its disease course, and outlines current barriers and potential future directions in this rapidly evolving field.
    Keywords:  diffusion magnetic resonance imaging; multiply myeloma; positron emission tomography computed tomography; whole-body imaging
    DOI:  https://doi.org/10.31083/BJHM50847
  9. Cancers (Basel). 2026 Feb 13. pii: 615. [Epub ahead of print]18(4):
      Recent implementations with novel target drugs of the hypomethylating agent/venetoclax doublet challenge our treatment approach in acute myeloid leukemia patients ineligible for intensive chemotherapy. Given the doublets' efficacy, associations of agents based on the disease's biology to the doublet backbone are leading to novel triplet (or more) combinations. In the present review mainly FLT3, IDH and KMT2A are discussed as possible targets in this context. These triplets do not only have efficacy in relapsed/refractory patients but also in treatment-naïve patients. Results from concluded and ongoing clinical trials, as well as real-world experiences, report high efficacies competing with intensive chemotherapy. For instance, the azacytidine/venetoclax/gilteritinib triplet as first-line is reported to induce a complete remission rate with and without incomplete recovery (CR/CRi) of 96%, with 90% of responders achieving minimal residual negativity. Once a stable CR was obtained, 47% of patients who were initially considered too frail for intensive chemotherapy were able to undergo allogeneic stem cell transplantation. However, there are still open questions and challenges regarding toxicity, post-remission therapy, and overall treatment duration. The present review will not only present the specific potency of these arising triplets, but also discuss their challenges and limitations, based on currently available data. Besides regimens containing approved inhibitors, triplets with next-generation inhibitors, including completely orally administered triplet regimens, are also summarized. Their promising results are leading to advanced phase clinical studies by international consortia and collaborative groups, aiming to further refine their clinical management.
    Keywords:  acute myeloid leukemia; hypomethylating agents; triplets; venetoclax
    DOI:  https://doi.org/10.3390/cancers18040615
  10. Haematologica. 2026 Feb 26.
      Despite advances in targeted therapies, relapsed/refractory B-cell non-Hodgkin lymphoma (R/R B-NHL) remains incurable in the majority of patients. Thus, there is a critical need to expand the treatment options for R/R B-NHL to improve patient outcomes. In this study, we characterized JNJ-80948543, a novel trispecific T-cell engager (TCE), designed to target CD79b+ and/or CD20+ lymphoma cells and bind to CD3 T cells with low affinity. By engaging two tumor-antigens, JNJ-80948543 may enhance tumor binding through avidity effects, potentially improving eradication of heterogeneous cell populations and reducing the risk of antigen escape. Preclinical data confirmed potent T-cell-mediated cytotoxicity against CD79b+ and/or CD20+ cells, with increased potency upon dual antigen engagement, consistent with an avidity effect. To mitigate cytokine release syndrome and T-cell exhaustion commonly associated with TCEs, JNJ-80948543 was designed with a low-affinity CD3 arm. In vitro, JNJ-80948543 achieved effective cytotoxicity with lower cytokine release compared to a matched high-affinity CD3 trispecific, JNJ-80948556. Despite reduced cytokine secretion by JNJ-80948543, both antibodies demonstrated comparable antitumor activity in xenograft mouse model. Collectively, the selectivity, potent cytotoxicity, tumor growth inhibition, and favorable cytokine profile of JNJ-80948543 supports its clinical development. Phase 1 clinical trials are ongoing to evaluate JNJ-80948543 as a monotherapy (NCT05424822) and in combination with a co-stimulatory bispecific antibody (NCT06139406) in patients with R/R B-NHL.
    DOI:  https://doi.org/10.3324/haematol.2025.288473
  11. Ann Pathol. 2026 Feb 26. pii: S0242-6498(26)00027-1. [Epub ahead of print]
      Recent advances in molecular pathology have profoundly reshaped the understanding and classification of mediastinal lymphomas, particularly primary mediastinal large B-cell lymphoma (PMBL) and mediastinal gray zone lymphoma (MGZL). These entities, long defined by morphological and immunophenotypic criteria, are now characterized by distinct genetic and transcriptional signatures. PMBL is defined by recurrent alterations involving CIITA, 9p24 (PD-L1/PD-L2), SOCS1, STAT6, and B2M, reflecting constitutive activation of the JAK/STAT and NF-κB pathways. Transcriptomic studies confirm its distinction from non-thymic diffuse large B-cell lymphomas (DLBCL) while revealing molecular overlaps with classical Hodgkin lymphoma (cHL). MGZL, on the other hand, exhibits intermediate and variable morphological and immunophenotypic features between PMBL and cHL, consistent with a shared thymic B-cell origin but divergent differentiation mechanisms. Alterations of PD-L1/PD-L2 have important prognostic implications, while circulating tumor DNA is emerging as a promising, non-invasive biomarker for molecular profiling and disease monitoring. Recent clinical studies have also led to significant therapeutic advances in PMBL, integrating molecular data into tailored treatment strategies and paving the way for precision medicine approaches in mediastinal lymphomas.
    Keywords:  FISH; Histologie; Histology; Lymphome B primitif du médiastin; Lymphome frontière du médiastin; Mediastinal gray zone lymphoma; Mutationnal profile; Primary mediastinal large B-cell lymphoma; Profil moléculaire
    DOI:  https://doi.org/10.1016/j.annpat.2026.02.006
  12. Blood Adv. 2026 Feb 24. 10(4): 1217-1232
       ABSTRACT: Diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) are the 2 most common B-cell lymphomas and are characterized by a dynamic crosstalk between tumor B cells and a heterogeneous, tumor-supportive microenvironment, such as immune, endothelial, and stromal components. Despite their recognized impact on the pathogenesis and prognosis of B-cell lymphoma, tumor-associated macrophages (TAM) have not been extensively explored in these diseases. In this study, we investigated mononuclear phagocyte (MNP) heterogeneity at the single-cell level and the activation profile of MNP, stromal, and endothelial compartments, in B-cell lymphoma lymph nodes compared to reactive secondary lymphoid organs. This was achieved using a combination of mass cytometry, single-cell RNA sequencing, in silico and spatial imaging approaches. Our findings revealed a lymphoma-specific pattern of TAM and blood endothelial cell (BEC) coactivation. Furthermore, we identified in DLBCL a spatial interaction between Annexin A1 (ANXA1)-expressing BEC and formyl-peptide receptor (FPR1/2) and S100A9-expressing monocytes/macrophages. This crosstalk is associated with an immunosuppressive tumor microenvironment and an adverse prognosis in patients with DLBCL.
    DOI:  https://doi.org/10.1182/bloodadvances.2024015689
  13. JCO Glob Oncol. 2026 Feb;12 e2500424
       PURPOSE: As there is a paucity of data comparing outcomes with different dosing regimens of PD-1 inhibitors in relapsed/refractory Hodgkin lymphoma (R/R HL), this retrospective analysis was undertaken to compare the efficacy of low-dose nivolumab (fixed at 40 mg) with the standard dose of 3 mg/kg.
    METHODS: Single-center retrospective analysis of patients with R/R HL who failed at least one salvage regimen and were treated with nivolumab between 2015 and 2023, at either 3 mg/kg (standard-dose nivolumab [SD-NIV]) or a flat dose of 40 mg (NIV40), both administered once in 2 weeks. Treatment response was assessed with 18F-labeled fluorodeoxyglucose-positron emission tomography-computed tomography after four doses of nivolumab.
    RESULTS: A total of 45 patients were included: 25 received 3 mg/kg (SD-NIV) and 20 received a flat dose of 40 mg (NIV40). The mean dose of nivolumab administered once in 2 weeks was 2.9 mg/kg (stable disease 0.31) in the SD-NIV group compared with 0.6 mg/kg (stable disease 0.10) in the NIV40 group (P < .001). Responses after four doses of nivolumab were similar in the SD-NIV versus NIV40 group: complete response (48% v 50%), partial response (12% v 10%), stable disease (20% v 20%), and progressive disease (20% v 20%; P = .997). Immune-related adverse effects were similar in the two groups (12% v 10%; P = .790). Two-year event-free survival (EFS) of the whole cohort treated with nivolumab with SD-NIV and NIV40 was 47% and 49.5%, respectively (P = .788). Twenty-two of the 45 patients underwent stem cell transplant (11 from each group), with a 2-year EFS of 90.1% versus 81.8% (P = .545) in the SD-NIV and NIV40 groups, respectively.
    CONCLUSION: Despite the inherent limitations of a retrospective analysis, the data suggests that nivolumab demonstrates biologic efficacy at doses as low as 0.6 mg/kg. Prospective trials comparing different dosing strategies are clearly warranted; such studies may facilitate approval of biologically active and cost-effective regimens, thereby broadening access to checkpoint inhibitors.
    DOI:  https://doi.org/10.1200/GO-25-00424
  14. Blood Adv. 2026 Feb 26. pii: bloodadvances.2026019625. [Epub ahead of print]
      For over two decades, the mevalonate pathway has been in focus as an interesting therapeutic target in the Philadelphia-chromosome negative myeloproliferative neoplasms (MPNs). Initially explored for its potential in cytoreductive and antithrombotic therapy, the role of statins in MPNs is now experiencing a compelling renaissance. This renewed interest is fueled by the recognition of MPNs as "a human inflammation model," driven by chronic inflammation that fuels clonal expansion, premature atherosclerosis, fibrogenesis, and an increased risk of second cancers and comorbidities. Statins possess a wide spectrum of pleiotropic effects beyond lipid-lowering, including anti-inflammatory, antiproliferative, pro-apoptotic, anti-angiogenic, and antifibrotic properties. They dampen the activation of leukocytes, platelets, and endothelial cells. Recent epidemiological studies from Denmark demonstrate that statins protect against the development of MPNs in the general population. Furthermore, emerging clinical data suggest that statins enhance the efficacy of interferon-alpha (IFN-α), the only known therapy capable of directly targeting the malignant stem cell and inducing minimal residual disease (MRD) in a subset of patients. This review traces the 20-year journey of the statin-in-MPN concept, from its mechanistic rationale to the present, where a confluence of evidence from comorbid disease prevention and onco-immunology is supportive of their upfront use. I posit that we are at a watershed moment, where statins should be integrated into the upfront treatment of MPNs and in combination therapy strategies, particularly with IFN-α, and potentially with ruxolitinib and metformin, to extinguish the chronic inflammatory drive and fundamentally alter the natural history of these neoplasms.
    DOI:  https://doi.org/10.1182/bloodadvances.2026019625
  15. Blood. 2026 Feb 26. pii: blood.2025031202. [Epub ahead of print]
      Altered lipid metabolism enables growth of acute myeloid leukemia (AML) cells. While mitochondrial lipid oxidation is well characterized, the contribution of peroxisomal fatty acid oxidation (pFAO) is unclear. In this study, we demonstrate that AML cells upregulate the peroxisomal very-long-chain fatty acid (VLCFA) transporter ABCD1 and increase endogenous levels of pFAO relative to healthy hematopoietic cells. Genetic silencing or pharmacological inhibition of ABCD1, with eicosenol, impairs pFAO causing accumulation of VLCFAs and selective AML cell death in vitro and in vivo. Loss of ABCD1 disrupts peroxisomal fatty acid import and lipid homeostasis in AML, while normal progenitors remain viable by upregulating glycolysis. In murine models, ABCD1 inhibition with eicosenol reduces leukemia burden and prolongs survival without toxicity. These findings identify ABCD1 as a regulator of pFAO and a novel anti-AML therapeutic target.
    DOI:  https://doi.org/10.1182/blood.2025031202
  16. Curr Issues Mol Biol. 2026 Feb 16. pii: 216. [Epub ahead of print]48(2):
      Multiple Myeloma is a malignancy of the plasma cells of the bone marrow. This cancer rapidly becomes refractory to many of the currently available chemotherapeutic regimens used against it, requiring an alternative option or supplementary therapy. Pterostilbene is a naturally occurring compound in a variety of commonly consumed plants that exhibits strong antioxidant properties and, lately, has shown increasing activity as an anti-neoplastic compound. A review of the literature published since 2015 on Google Scholar and PubMed was conducted, with a focus on randomized controlled trials and an exclusion of review articles, unless pertinent to pathophysiology of Multiple Myeloma or background on Pterostilbene as a compound. Though data is limited in the use of Pterostilbene as an agent to combat Multiple Myeloma, studies have shown that it, along with synthetic derivatives, can induce apoptosis and limit proliferation of Multiple Myeloma cell lines. While safety has been evaluated in several settings with promising results, for Pterostilbene to be considered as a supplementary treatment in Multiple Myeloma, safe and effective doses of the compound in this patient population must be investigated and established via pre-clinical and clinical trials in the future.
    Keywords:  antioxidant; chemotherapy; hematology; multiple myeloma; oncology
    DOI:  https://doi.org/10.3390/cimb48020216
  17. Eur J Haematol. 2026 Feb 24.
      Extramedullary disease (EMD) of multiple myeloma (MM) is a critical indicator of disease progression, with a complex pathophysiology involving tumor microenvironment dysregulation, chromosomal abnormalities, and aberrant signaling pathway activation. Advances in detection technologies have significantly improved EMD diagnosis rates in recent years, but clinical treatment still faces challenges such as high drug resistance rates and difficulties in managing lesions at specific sites. This article systematically reviews the definition, classification, biological characteristics, pathophysiological mechanisms, diagnostic methods, current treatment strategies, and emerging therapeutic challenges of EMD. It emphasizes the interactions between different pathogenic factors and the heterogeneous therapeutic responses of various EMD subtypes, aiming to provide a comprehensive reference for clinical practice and research directions.
    Keywords:  CAR‐T; extramedullary disease; extramedullary plasmacytoma; multiple myeloma; targeted therapy
    DOI:  https://doi.org/10.1111/ejh.70145
  18. Hematol Oncol. 2026 Mar;44(2): e70181
      
    Keywords:  CLL; artificial intelligence; chronic lymphocytic leukemia; consensus; delphi study; ibrutinib; venetoclax
    DOI:  https://doi.org/10.1002/hon.70181