bims-hemali Biomed News
on Hematologic malignancies
Issue of 2026–02–22
27 papers selected by
Alexandros Alexandropoulos, Γενικό Νοσοκομείο Αθηνών Λαϊκό



  1. Blood Adv. 2026 Feb 17. pii: bloodadvances.2025018537. [Epub ahead of print]
      The IMS and IMWG recently published a new consensus genomic staging (CGS) for defining high-risk (HR) newly diagnosed multiple myeloma (NDMM) patients, intended to provide consistency in clinical trial reporting and for use in designing enrichment clinical trials focused on the HR subset. The HR definition is the first to include TP53 mutations and considers the co-occurrence of IgH translocations with chromosome 1 aberrations. Given that limited data from the anti-CD38 monoclonal antibody-based quadruplet induction regimens were available for consensus consideration, here, we demonstrate that the new HR definition also predicts clinical outcomes in this setting. The patient population was 503 NDMM patients treated with daratumumab-based quadruplet induction therapy at Memorial Sloan Kettering Cancer Center, with a median follow-up time of 2.2 years, (maximum 7.9 years). The CGS criteria defined 31% of patients as HR, better delineating patients at intermediate risk by pre-existing prognostic scores. The CGS did not predict early minimal-residual disease (MRD) status, with MRD-negativity occurring at the same rate in HR and standard risk (SR) patients. However, the CGS did predict progression-free survival (PFS), which was a median of 2.6 years in HR compared with not reached in SR (p<0.0001). CGS risk remained predictive of PFS even in the setting of MRD-negativity following autologous stem cell transplantation. We conclude that while the IMS-IMWG CGS is ideal for standardizing NDMM trial design, any MRD-guided trial design should also consider genomic risk.
    DOI:  https://doi.org/10.1182/bloodadvances.2025018537
  2. Blood Adv. 2026 Feb 20. pii: bloodadvances.2025019050. [Epub ahead of print]
      Belantamab mafodotin (belamaf), an antibody-drug conjugate targeting B-cell maturation antigen, has demonstrated single-agent activity in relapsed/refractory multiple myeloma (RRMM) but is associated with ocular toxicity. This phase 1/2 study evaluated the safety and preliminary efficacy of belamaf administered every 8 weeks in combination with carfilzomib, lenalidomide, and dexamethasone (KRd-b) in patients with RRMM. Eligible patients had received at least one prior line of therapy and had not progressed on full-dose lenalidomide. In the dose-escalation phase (3+3 design), belamaf was administered at 1.4 or 1.9 mg/kg every 8 weeks. The recommended phase 2 dose was 1.9 mg/kg, with no dose-limiting toxicities at this level. Among 19 patients treated, the overall response rate was 89.5%, and 78.9% achieved very good partial response or better, with minimal residual disease negativity in all complete responders. At a median follow up of 19.3 months, 24-month progression-free survival and overall survival rates were 74.3% and 85.1%, respectively. Keratopathy occurred in 94.7% of patients but was mostly grade 1-2, reversible, and manageable without permanent discontinuation. Grade ≥3 keratopathy (31.6%) was comparable to historical rates despite the less frequent dosing. Other adverse events, including hematologic and gastrointestinal toxicities, were manageable and consistent with known profiles of KRd or belamaf. The combination demonstrated deep and durable responses, including in high-risk and lenalidomide maintenance dose-refractory patients. These results support the feasibility of KRd-b with extended-interval belamaf and warrant further evaluation in phase 2 trials to confirm its clinical benefit in RRMM. This trial is registered at www.clinicaltrials.gov as NCT04822337.
    DOI:  https://doi.org/10.1182/bloodadvances.2025019050
  3. Blood. 2026 Feb 19. 147(8): 802-804
      
    DOI:  https://doi.org/10.1182/blood.2025031561
  4. Expert Rev Clin Immunol. 2026 Feb 18.
       INTRODUCTION: Bruton's tyrosine kinase inhibitors (BTKi) have transformed the management of B-cell malignancies by selectively targeting signaling pathways essential for malignant B-cell survival, thereby reducing the systemic toxicity of conventional chemotherapy. However, with their expanding use, cutaneous adverse events are increasingly recognized as clinically relevant complications that may affect quality of life and treatment adherence.
    AREAS COVERED: This review provides an updated overview of first- and second-generation BTKi, including ibrutinib, acalabrutinib, zanubrutinib, and pirtobrutinib, with a specific focus on dermatologic toxicities. A comprehensive literature search was conducted using PubMed, Embase, and Scopus, covering publications up to February 2025. Clinical studies, case series, and case reports describing skin-related adverse events associated with BTKi therapy were reviewed.
    EXPERT OPINION: Cutaneous toxicities related to BTKi are often underrecognized but clinically significant, ranging from xerosis and bruising to lichenoid eruptions and vasculitis. First-generation agents, particularly ibrutinib, are associated with a broader spectrum of dermatologic adverse events, whereas newer BTKi show improved selectivity and potentially reduced skin toxicity. Early recognition, standardized dermatologic evaluation, and proactive multidisciplinary management are essential to minimize patient discomfort, preserve quality of life, and prevent unnecessary treatment discontinuation.
    Keywords:  Bruton tyrosine kinase inhibitors; cutaneous toxicities; hematological malignancies; oncodermatology; targeted therapy toxicity
    DOI:  https://doi.org/10.1080/1744666X.2026.2634839
  5. Ann Hematol. 2026 Feb 21. pii: 132. [Epub ahead of print]105(4):
      It is widely acknowledged that B-cell lymphoma represent a significant threat to human health, and Bruton Tyrosine Kinase inhibitors (BTKi) have been shown to exhibit superior clinical efficacy and safety in comparison to conventional chemotherapy and immunotherapy modalities. However, as patients continue to use BTKi over a time, they will inevitably encounter the drug resistance. This resistance renders the therapeutic efficacy of BTKi, thereby significantly constraining its clinical benefits. Drug resistance of tumor is a multifaceted process influenced by numerous factors, mainly including individual genetic variations, tumor stem cells, drug inactivation, reduced drug absorption, and altered metabolism of anti-tumor drugs. The tumor microenvironment (TME) has been demonstrated to exert an important influence on the process of therapy resistance. It is evident that non-cellular components (e.g. the extracellular matrix, hypoxia, an acidified microenvironment, exosome, and cytokines) modulate the drug resistance through different mechanisms. These mechanisms include physical barriers that impede drug delivery, the formation of an immunosuppressive microenvironment, metabolic reprogramming and the activation of bypass signal moueculars. Furthermore, the presence of mutations of moleculars involved in the BCR signaling pathways (e.g. BTK and PLCG2 mutations) and the aberrant activation of key pathways such as PI3K-AKT-mTOR, NF-κB, Wnt/β-catenin and MAPK/ERK signaling further weakened the efficacy of BTKi. This review focus on the mechanism of BTKi resistance, the role of the TME and its components in drug resistance. It emphasized that targeting TME remodeling and combined the inhibition of multiple pathways may provide a new strategy for overcoming drug resistance, optimizing the treatment paradigm of B-cell lymphoma.
    Keywords:  B-cell lymphoma; BKTi; Drug resistance; Tumor microenvironment (TME)
    DOI:  https://doi.org/10.1007/s00277-026-06775-x
  6. J Cell Mol Med. 2026 Feb;30(4): e71053
      Resistance to tyrosine kinase inhibitors (TKIs) remains a major challenge in breakpoint cluster region (BCR)::Abelson 1 (ABL1)-driven leukaemias. Asciminib offers a novel therapeutic option; however, resistance continues to emerge. We hypothesised that targeting proteostasis and epigenetic regulation with bortezomib and panobinostat could eliminate TKI-refractory cells via TKI-independent mechanisms. We profiled parental and TKI-resistant chronic myelogenous leukaemia (CML) and Ba/F3 models. Viability, cytotoxicity, and caspase-3/7 activity were assessed following single-agent treatment with asciminib, ponatinib, bortezomib, or panobinostat. The effects of the bortezomib-panobinostat combination on colony formation, mitochondrial membrane potential, and apoptosis were evaluated. Asciminib showed reduced potency in resistant models and a right-shifted dose-response curve in T315I cells, whereas ponatinib retained activity across BCR::ABL1 variants. Bortezomib and panobinostat induced low-nanomolar cytotoxicity and robust caspase-3/7 activation in resistant lines. The combination of bortezomib and panobinostat showed modest trends toward reduced cell viability and increased cytotoxicity and caspase-3/7 activity, especially in TKI-resistant cells. The combination suppressed clonogenic growth and triggered apoptosis in resistant cells. Co-inhibition of proteasomes and histone deacetylases eliminates TKI-refractory BCR::ABL1-driven leukaemia cells by inducing mitochondrial apoptosis and loss of clonogenic potential. These findings indicate a clinically actionable, TKI-independent strategy for the salvage treatment of multidrug-resistant CML.
    Keywords:  BCR::ABL1; CML; HDAC; apoptosis; asciminib resistance; bortezomib; panobinostat; proteostasis
    DOI:  https://doi.org/10.1111/jcmm.71053
  7. Br J Haematol. 2026 Feb 15.
      Despite the improvement in outcomes of patients with newly diagnosed multiple myeloma (NDMM) with quadruplet therapy (QUAD) and autologous stem cell transplantation (ASCT), outcomes are heterogeneous. The International Myeloma Society (IMS) and International Myeloma Working Group (IMWG) published new consensus high-risk (new-HiR) criteria which combine cytogenetic abnormalities, next-generation sequencing data, β2 microglobulin and renal function developed in a population treated prior to the introduction of QUADs. We utilized a cohort of NDMM patients treated with QUAD + ASCT with a median follow-up of 41.5 months to validate the IMS/IMWG high-risk criteria and compared the performance of the old-HiR, based on the presence of t(4;14), t(14;16) or del(17p) versus new-HiR criteria. Among the 310 patients, 89 (29%) were classified as new-HiR. Patients with new-HiR NDMM had substantially worse progression-free survival (PFS) (hazard ratio [HR] 4.17, 95% confidence interval [CI] 2.58-6.73; p < 0.001) and overall survival (OS) (HR 5.13, 95% CI 2.44-10.80, p < 0.001). The new IMS/IMWG criteria better fit a predictive model for PFS and OS than the old criteria. The new criteria were able to identify misclassified patients under the old criteria. The 2025 IMWG/IMS criteria outperform legacy risk classification systems in the identification of patients at high risk for early progression and death despite modern therapy.
    Keywords:  multiple myeloma; risk stratification; stem cell transplant
    DOI:  https://doi.org/10.1111/bjh.70359
  8. Blood Adv. 2026 Feb 18. pii: bloodadvances.2025018455. [Epub ahead of print]
      Few prospective benchmark studies exist to characterize the evolving contemporary real-world practice for PTCL. We report the patterns of first-line care and outcomes for 720 patients with systemic PTCL enrolled in two related prospective cohort studies, LEO from 2015-2020 (ClinicalTrials.gov NCT02736357) and MER from 2002-2015, both followed through 2024. The primary endpoints were EFS and OS using Kaplan-Meier estimator and Cox regression model. Secondary endpoints included correlations of clinical and treatment factors with survival. The most common induction regimens were CHOP-based (70%), given as CHOP (36%), CHOP plus etoposide (23%), or CHOP-like plus novel agents (11.5%, including 5% BV-CHP). Consolidative autologous stem cell transplant was performed in 102 patients (14%). Within nodal PTCL, EFS and OS were adversely associated with IPI 2-5 (HR=2.00, 95%CI: 1.59-2.52 for EFS; HR=2.44, 95%CI: 1.86-3.19 for OS), PIT 1-4 (HR=3.02, 95%CI 2.07-4.39 for EFS; HR=5.10, 95%CI 3.01-8.63 for OS), and non-ALCL subtypes (HR=2.97, 95%CI: 2.26-3.91 for EFS; HR=3.71, 95%CI: 2.65-5.20 for OS). Within LEO, which captured increasing first-line etoposide and BV, adding etoposide to CHOP was associated with better OS in ALK-negative ALCL (HR=0.14, 95%CI: 0.03-0.69, p=0.015). BV-CHP showed a trend toward OS improvement in ALCL (HR=0.15, 95%CI 0.02-1.19, p=0.073). Patients failing EFS6 and EFS24 had 5-year subsequent OS of 12% (95% CI: 7.8%, 19%) and 17% (95% CI: 13%, 22%), respectively. The inferior outcomes in non-ALCL subtypes and patients failing EFS6 and EFS24 highlight unmet needs with CHOP-based induction, where clinical trials with targeted therapy should be prioritized.
    DOI:  https://doi.org/10.1182/bloodadvances.2025018455
  9. Ann Oncol. 2026 Mar;pii: S0923-7534(26)00017-7. [Epub ahead of print]37(3): 284-285
      
    DOI:  https://doi.org/10.1016/j.annonc.2026.01.008
  10. Cell Rep Med. 2026 Feb 17. pii: S2666-3791(26)00045-5. [Epub ahead of print] 102628
      Multiple myeloma (MM), the second most common hematologic malignancy, remains incurable, highlighting the need for durable therapies. Natural killer (NK) cell engagers (NKCEs) represent a promising alternative to T cell therapies, offering potent anti-tumor activity with limited cytokine release. SAR445514 (SAR'514) is a trifunctional NKCE that co-engages NKp46 and FcγRIIIa to activate NK cells while targeting B cell maturation antigen (BCMA) on MM cells. After exploring several molecular formats with varied BCMA and NKp46 valency, we selected SAR'514, a monovalent format with enhanced antibody-dependent cellular cytotoxicity (ADCC). SAR'514 has potent and selective anti-tumor activity in vitro and in vivo, outperforming other FcγRIIIa-immune cell engagers, while inducing minimal cytokine release compared to T cell engagers targeting the same antigen. Ex vivo, SAR'514 efficiently activates NK cells from MM patients and induces cytotoxicity against autologous malignant cells, including those resistant to standard therapies. These findings support further development of SAR'514.
    Keywords:  BCMA; NK cell engager; anti-tumor activity; ex-vivo bone marrow; multiple myeloma; preclinical model; trifunctional antibody
    DOI:  https://doi.org/10.1016/j.xcrm.2026.102628
  11. Ann Med. 2026 Dec;58(1): 2626141
       BACKGROUND AND OBJECTIVE: Acute Leukemia (AL) diagnosed during pregnancy is uncommon, and the management of AL complicated by pregnancy is a poorly studied area that faces a therapeutic dilemma.
    METHOD: 23 cases diagnosed with AL during pregnancy were collected from our center between 2012 and 2022. Additionally, we summarized 17 clinical studies on AL diagnosed during pregnancy.
    RESULT: Sixteen AML and seven ALL patients were diagnosed during pregnancy in our center; most patients diagnosed during the first or second trimester tended to receive chemotherapy after abortion. All patients diagnosed during the third trimester opted to defer therapy until after delivery. The rate of overall response rate (ORR) was 77.3%, which was found to be similar to that of the general population. A Short delay in initiating anti-leukemia treatment is not associated with a negative impact on prognosis. We conducted a meta-analysis of the literature, and the summary relative complete remission (CR) rate was 76.9% (95%CI 69.1-84.6%) (Random Effects Model I^2 = 66%, p <0.001). We included four Chinese studies comprising 135 participants for further analysis. For non-M3 AL patients, CR rate of the chemotherapy-first cohort was 63.6%, compared with 68.6% in the treatment-after-delivery or abortion cohort (p = 0.657). For M3 patients, the rate was 100 and 83.3%, respectively (p < 0.001).
    CONCLUSION: Our findings suggest that for non-M3 AL patients can sometimes be managed during pregnancy. For M3 patients, early treatment potentially yield favorable outcomes for both the mother and fetus, using ATRA-based regimens without arsenic trioxide (in the second and third trimester) or standard chemotherapy (in the second trimester) may be considered a treatment option.
    Keywords:  Pregnancy; acute leukemia; delivery; maternal and fetal outcome
    DOI:  https://doi.org/10.1080/07853890.2026.2626141
  12. Leukemia. 2026 Feb 17.
      Acute myeloid leukemia (AML) is an aggressive myeloid malignancy with a poor prognosis. Venetoclax (Ven), a BCL2 inhibitor, has shown promising results but often leads to relapse due to mitochondrial dysregulation, particularly due to upregulation of the anti-apoptotic protein MCL1. Overexpression of the transcription factor STAT3 has been linked to poor survival in AML patients. Overexpression of STAT3 in a transgenic murine model induces a myeloid malignancy with a short latency period and inflammatory upregulation. The current study identifies STAT3 upregulation as a key mechanism of Ven resistance. A clinically relevant STAT3 degrader effectively reduces both total and phosphorylated STAT3, corrects mitochondrial structural and functional dysregulation, and induces apoptosis in Ven-resistant AML cell lines. KT-333 significantly decreases STAT3 and MCL1 protein levels and improves survival in Ven-resistant (Ven-Res) AML murine models. In summary, STAT3 hyperactivation is leukemogenic, is further potentiated in Ven-resistance and can be clinically targeted with a novel and specific STAT3 degrader. Pictorial representation depicting upregulation of STAT3 and MCL1 in venetoclax resistant myeloid malignancies such as MDS and AML causing mitochondrial structural abnormalities and dysfunction. By using specific STAT3 degrader, STAT3 inhibition, and thereby indirect downregulation of MCL1 can be a promising therapeutic intervention to target drug resistant clones in MDS and AML.
    DOI:  https://doi.org/10.1038/s41375-026-02883-9
  13. Hemasphere. 2026 Feb;10(2): e70319
      The cellular composition of the chronic myeloid leukemia (CML) bone marrow (BM) beyond granulocyte enrichment remains poorly understood. We analyzed 1548 routinely stained BM aspirate slides from 598 patients across seven sites using deep learning-based image analysis to identify cytomorphological markers predictive of major molecular response. Erythroid precursor enrichment, monocyte nuclear lobulation, and low peripheral leukocyte count were associated with improved tyrosine kinase inhibitor (TKI) response. These features were validated both visually and computationally in two independent cohorts. We developed a Morphoclinical model integrating these image-derived and clinical variables, outperforming (area under the receiver-operating curve [AUROC] 0.76) the clinically used EUTOS long-term survival score (AUROC 0.53) and BCR::ABL1 halving time (AUROC 0.61). Notably, poor-risk patients treated with second-generation TKIs achieved outcomes similar to favorable-risk patients on imatinib. These results underline the overlooked prognostic value of BM cytomorphology to refine risk stratification and support more personalized frontline therapy in CML.
    DOI:  https://doi.org/10.1002/hem3.70319
  14. Cancer. 2026 Feb 15. 132(4): e70293
       BACKGROUND: POEMS syndrome is a rare hematologic condition with no established standard of therapy. Bortezomib, a proteasome inhibitor, has shown potential to offer significant clinical benefits for patients with newly diagnosed POEMS syndrome. However, comprehensive data on its long-term efficacy remain scarce. This study aimed to assess the long-term efficacy of bortezomib-based regimens for newly diagnosed POEMS syndrome.
    METHODS: A total of 53 patients were enrolled in this study. Fluorescence in situ hybridization analysis was performed on CD138-selected bone marrow samples. All patients received bortezomib-based regimens as first-line therapy. Hematologic responses, vascular endothelial growth factor (VEGF) levels, neurological response rates, and long-term survival outcomes were evaluated.
    RESULTS: Patients received a median of four treatment cycles, with a median follow-up time of 92.4 months. Hematologic responses were evaluable in 42 patients, yielding an overall response rate was 85.7%, including a complete response rate of 64.3%. VEGF responses were assessed in 44 patients, with an overall response rate of 88.6% and a complete response rate of 56.8%. Median VEGF levels decreased from 944.4 pg/mL to 137.8 pg/mL. Neurological improvements were observed in 90.6% of patients, with 24.5% achieving a complete neurological response. Median overall survival (OS) and progression-free survival were not reached. The 5-year OS and progression-free survival rates were 83.0% and 67.4%, respectively. Fluorescence in situ hybridization analysis identified 1q21 gain as the most frequent abnormality in this cohort, and it was an independent prognostic factor for OS.
    CONCLUSIONS: Bortezomib-based regimens were effective and achieved favorable long-term survival outcomes for patients with newly diagnosed POEMS syndrome.
    Keywords:  FISH; POEMS; bortezomib
    DOI:  https://doi.org/10.1002/cncr.70293
  15. Neurol Neurochir Pol. 2026 Feb 17.
      Primary central nervous system lymphoma (PCNSL) is an aggressive malignancy, which is challenging to diagnose, often leading to delays in treatment initiation. The gold standard for diagnosis is brain biopsy, an invasive technique with a risk of neurologic compromise, and in some cases, biopsy may not be feasible or safe. Thus, there have been significant efforts to develop less invasive methods of diagnosis, particularly utilizing cerebrospinal fluid (CSF). Liquid diagnostics is an emerging area of research in many types of cancer, particularly central nervous system (CNS) tumors. Standard CSF cytology and flow cytometry lack sufficient sensitivity; however, the identification of specific biomarkers, particularly genomic variants such as the MYD88 L265P mutation, which can be detected in circulating tumor DNA (ctDNA), has demonstrated increasing promise as a diagnostic tool for PCNSL. Here, we review key advancements in the field of liquid diagnostics for PCNSL, and their potential to reform the approach to diagnosis.
    Keywords:  CSF biomarkers; MYD88; circulating tumor DNA; liquid diagnostics; primary central nervous system lymphoma
    DOI:  https://doi.org/10.5603/pjnns.109853
  16. Front Immunol. 2026 ;17 1741042
       Background: Thrombopoietin receptor agonists combined with anti-thymocyte globulin (ATG) and cyclosporine (CsA) are the standard immunosuppressive therapy (IST) for severe/very severe aplastic anemia (SAA/VSAA). However, early response rates remain suboptimal. Cyclophosphamide (CTX) has shown efficacy in relapsed/refractory AA. Therefore, we designed a clinical trial to evaluate low-dose CTX combined with the standard IST as a first-line treatment for SAA/VSAA to improve early response rates.
    Methods: This study was a single-arm, prospective, phase II clinical trial using a Simon's two-stage design, and 43 patients were enrolled. The primary endpoint was the overall response rate (ORR) at 3 months. Newly diagnosed SAA/VSAA patients received a combination treatment as follows: porcine ATG at 25 mg/kg/day from days 1 to 5, CsA at 3-5 mg/kg/day continuously, hetrombopag at 15 mg/day starting from day 1 and continued for 6 months, low-dose CTX at 20 mg/kg/day on days 29-30 and days 43-44.
    Results: All 43 patients achieved the primary endpoint, demonstrating 3-month and 6-month ORR of 65.1% (28/43) and 69.8% (30/43) respectively. Complete response (CR) rates were 9.3% (4/43) at 3-month and 27.9% (12/43) at 6-month. CTX associated toxicities comprised 100% grade 1-2 gastrointestinal reactions, grade 3-4 neutropenia in 62.8% of patients (median duration 6 days, range 4-33). Infectious events occurred in 60.5% (26/43) of patients within the first 3 months of treatment, while no mortality observed during this period.
    Conclusions: Low-dose CTX combined with standard IST appears to improve the early response rate in SAA/VSAA patients with manageable toxicity.
    Keywords:  anti-thymocyte globulin; cyclophosphamide; immunosuppressive therapy; sever aplastic anemia; thrombopoietin receptor agonists
    DOI:  https://doi.org/10.3389/fimmu.2026.1741042
  17. Leukemia. 2026 Feb 17.
      Multiple myeloma (MM) resistant to CD38 antibodies, two immunomodulatory drugs (IMiDs), two proteasome inhibitors (PIs), and both BCMA- and GPRC5D-directed immunotherapies defines hepta-refractory MM, a novel end-stage entity. In a multi-center cohort of 37 patients, median overall survival was 12.8 months, with progression-free survival across salvage therapy lines of only 2.7-3.7 months. Whole genome sequencing (WGS) revealed frequent biallelic tumor suppressor gene events, particularly TP53, consistent with proliferative, apoptosis-resistant disease. Genomic alterations linked to IMiD, BCMA, GPRC5D, and CD38 resistance occurred in 71%, 41%, 35%, and 12% of patients, respectively. Almost one-third of patients showed concurrent loss of BCMA (TNFRSF17) and GPRC5D. Sequential WGS demonstrated branching evolutionary trajectories with multiple distinct TNFRSF17 and GPRC5D variants arising within individual patients, pointing to a hidden reservoir of persistent clones with ongoing mutational processes even after deep remissions. Immunohistochemistry (IHC) confirmed loss of BCMA expression caused by biallelic TNFRSF17 genomic events but also revealed loss of expression attributable to other mechanisms. Importantly, BCMA status predicted benefit from BCMA re-treatment. Hepta-refractory MM is marked by profound genomic complexity, antigen loss, and poor outcomes, highlighting the need for novel therapies and broader diagnostics such as integrated genomic and IHC testing for this ultra-refractory population.
    DOI:  https://doi.org/10.1038/s41375-026-02889-3