bims-tremyl Biomed News
on Therapy resistance biology in myeloid leukemia
Issue of 2025–10–19
twenty-one papers selected by
Paolo Gallipoli, Barts Cancer Institute, Queen Mary University of London



  1. Lancet Haematol. 2025 Oct 08. pii: S2352-3026(25)00254-6. [Epub ahead of print]
       BACKGROUND: Enasidenib, a mutant IDH2 inhibitor, is used to treat IDH2-mutated acute myeloid leukaemia (AML). Preclinical studies have demonstrated synergy between enasidenib and venetoclax, a BCL2 inhibitor, in IDH2-mutated AML. The aim of this study was to evaluate the safety and activity of enasidenib plus venetoclax in patients with relapsed or refractory IDH2-mutated AML or myelodysplastic syndromes (MDS).
    METHODS: The ENAVEN-AML study was a single-arm, phase 1b/2 trial conducted at two centres in Canada. Patients were eligible to participate if they were 18 years or older, had an Eastern Cooperative Oncology Group performance status of 0 to 2, had a confirmed IDH2 mutation (affecting Arg140 or Arg172), and had AML or MDS that was refractory or had relapsed after at least one line of treatment. Patients were treated with venetoclax 400 mg orally daily with a 3-day dose ramp-up starting on cycle 1 day 1 and enasidenib 100 mg orally daily starting on cycle 1 day 15. The primary endpoint of the phase 1b portion was safety, which included dose-limiting toxicity and the frequency and severity of treatment-emergent adverse events (TEAEs), as well as determining the maximum tolerated dose and recommended phase 2 dose. The primary objective of the phase 2 portion was to assess preliminary activity, with overall response rate by intention-to-treat as the primary endpoint. Assessment of safety and activity were determined on the pooled analysis data from the phase 1 and 2 studies. The ENAVEN-AML study is registered with ClinicalTrials.gov (NCT04092179) and is completed.
    FINDINGS: From Nov 12, 2020, to July 5, 2022, the study enrolled 27 patients (13 in phase 1b, 14 in phase 2) and the median follow-up was 20·2 months (IQR 15·0-23·0) at the data cutoff on Sept 30, 2023. The median age was 70 years (IQR 55-76); 16 (59%) of 27 patients were male, 11 (41%) female, and 19 (70%) White. 26 patients had relapsed or refractory AML, and one patient had relapsed MDS. The most common grade 3 or worse TEAEs were febrile neutropenia (n=11, 41%), infections (n=8, 30%), thrombocytopenia (n=7, 26%), pneumonia (n=6, 22%), sepsis (n=5, 19%), and anaemia (n=5, 19%). One case of IDH inhibitor-associated differentiation syndrome was observed. Serious adverse events were reported in 17 (62%) of 27 patients, most commonly infections (n=11, 41%) and intracranial bleeding (n=5, 19%). No dose-limiting toxicities or treatment-related deaths were observed. The recommended phase 2 dose was 400 mg daily for venetoclax and 100 mg daily for enasidenib. Of the 26 patients with AML, the overall response rate was 62% (95% CI 41-80; 16 of 26), with 13 (50%) of 26 having complete remission. The only patient with MDS did not respond to enasidenib plus venetoclax.
    INTERPRETATION: Enasidenib plus venetoclax is safe, with no unexpected TEAEs or treatment-related deaths, and shows preliminary activity in patients with relapsed or refractory IDH2-mutated AML and MDS.
    FUNDING: AbbVie and Bristol Myers Squibb.
    DOI:  https://doi.org/10.1016/S2352-3026(25)00254-6
  2. Semin Hematol. 2025 Sep 13. pii: S0037-1963(25)00038-1. [Epub ahead of print]
      After decades of therapeutic inertia, the treatment of acute myeloid leukemia (AML) has seen remarkable improvements over the past ten years. Scientific discoveries have substantially enhanced the understanding of AML disease biology. The improved knowledge about leukemic transformation and disease mechanisms in this heterogeneous group of aggressive blood cancers has resulted in enhanced biologically defined risk prognostication and the development of novel targeted therapeutic agents. Many of these mechanism-based therapeutics have entered clinical development, with some getting approval for the treatment of specific genetically defined AML subgroups in patients fit or unfit for intensive chemotherapy-based treatment. As a result, the European LeukemiaNet (ELN) expert panel has established a distinct genetic risk stratification for AML patients undergoing less-intensive treatment, which incorporates targeted drugs (ELN 2024). The ELN 2022 risk categories, designed for predicting outcomes following intensive chemotherapy, did not adequately assess responses to these new regimens. In this review, we discuss the current state-of-the-art approaches in both intensive and less-intensive front-line treatments for AML, highlighting the most promising therapeutic innovations.
    Keywords:  AML; Intensive treatment; Less intensive treatment; Leukemia therapy; Targeted drugs
    DOI:  https://doi.org/10.1053/j.seminhematol.2025.09.001
  3. Bone Marrow Transplant. 2025 Oct 15.
      Outcomes in myelofibrosis (MF) patients undergoing allogeneic hematopoietic cell transplantation (allo-HCT) appear unaffected by the intensity of the preparative regimen, defined traditionally as myeloablative (MAC) or reduced intensity conditioning (RIC). The Transplant Conditioning Intensity (TCI) index is an objective tool offering a precise measure of conditioning intensity. We explored the potential association between TCI score and overall survival (OS), progression-free survival (PFS), cumulative incidence of relapse (CIR) and non-relapse mortality (NRM) in 2454 MF patients undergoing allo-HCT between 2012 and 2021, selected from the EBMT registry. Patients receiving TCI-intermediate/high regimens had similar OS (HR 1.12, 95% CI 0.97-1.30) and PFS (HR 1.00, 95% CI 0.88-1.14) compared to TCI-low regimens. However, TCI-intermediate/high regimens were associated with lower risk of relapse (HR 0.74, 95% CI 0.61-0.91, p = 0.008) and higher risk of NRM (HR 1.24, 95% CI 1.04-1.48, p = 0.02). Our findings suggest that the TCI score provides a more clinically relevant stratification of conditioning intensity than the conventional MAC/RIC classification. While higher intensity TCI regimens are associated with lower RI, this benefit is offset by increased NRM, resulting in no survival advantage. However, the TCI index may enable a more personalized approach to conditioning regimen selection by balancing relapse risk with patient frailty.
    DOI:  https://doi.org/10.1038/s41409-025-02732-w
  4. Blood. 2025 Oct 17. pii: blood.2025029011. [Epub ahead of print]
      The BCR::ABL1 tyrosine kinase inhibitors (TKIs) in CML represent a paradigm for molecularly targeted therapy. However, clinical outcomes - rate/depth of response, treatment-free remission (TFR), progression to blast crisis (BC) - and adverse events vary among patients. While additional somatic mutations have been invoked to explain varying clinical outcomes, we here propose a complementary perspective based on single-cell omics approaches that have enabled unprecedented resolution of the cellular ecosystems, including their composition, interactions, and activity. In treatment-naïve chronic phase (CP) patients, this has revealed differences in the growth-rate of BCR::ABL1+ clones, ratio of TKI-insensitive leukemic stem cells (LSCs) to residual hematopoietic stem cells (HSCs), and immune cell composition - factors that collectively contribute to variability in therapy efficacy. Together these findings suggest that cellular heterogeneity serves as a foundation of clinical outcome in CML. Patients who remain in CP exhibit an erythroid signature in LSCs, while those progressing to BC manifest an inflammatory profile, additional mutations, and expansion of early progenitors. Deep responders with active natural killer, and regulatory T-cells are more likely to sustain TFR. Similarly, the outcomes of donor lymphocyte infusion after allogenic stem cell transplantation are heterogenous and reflect differences in pre-existing T-cell clonotypes, their expansion and interaction with leukemic cells in responders versus non-responders. Here, we summarize key insights from sc-omics in CML and propose an actionable roadmap to further leverage these technologies. This includes mechanistically explaining heterogeneity, predicting therapy response and BC, tracking leukemogenic clones longitudinally, targeting TKI-insensitive LSCs, and restoring hematopoiesis from residual HSCs.
    DOI:  https://doi.org/10.1182/blood.2025029011
  5. Haematologica. 2025 Oct 16.
      Frontline use of the BCL2 inhibitor, venetoclax, for acute myeloid leukemia (AML) has resulted in broad improvements in patient outcome. A major remaining challenge is the development of venetoclax resistance, frequently driven by compensatory transcriptional programs that promote cell survival and differentiation. These changes reduce dependence on BCL2 in favor of alternative anti-apoptotic BCL2 family members such as MCL1 or BCL2L1 (BCL-XL). Using CRISPR-based genome-wide perturbation screens, we investigated the genetic dependencies of venetoclax and the BCL2/BCL2L1 dual inhibitor AZD4320. We identified the N6-methyladenosine (m6A) writer RBM15, and the Nucleosome Remodeling and Deacetylase (NuRD) complex interactor ZMYND8 as novel mediators of resistance to both venetoclax and AZD4320. Loss of RBM15 or ZMYND8 induced drug resistance, concurrent with alterations in BCL2 family expression and monocytic differentiation. Accordingly, in AML patient samples we found reduced expression of the respective m6a or NuRD complexes was significantly associated with monocytic differentiation and ex vivo resistance to the same drugs. These findings provide critical insights into previously undescribed mechanisms of BCL2 family inhibitor resistance in AML.
    DOI:  https://doi.org/10.3324/haematol.2025.287972
  6. Nat Commun. 2025 Oct 16. 16(1): 9194
      Clonal hematopoiesis (CH) is defined by the expansion of a lineage of genetically identical cells in blood. Genetic lesions that confer a fitness advantage, such as leukemogenic point mutations or mosaic chromosomal alterations (mCAs), are frequent mediators of CH. However, recent analyses of both single cell-derived colonies of hematopoietic cells and population sequencing cohorts have revealed CH frequently occurs in the absence of known driver genetic lesions. To characterize CH without known driver genetic lesions, we use 51,399 deeply sequenced whole genomes from the NHLBI TOPMed sequencing initiative to perform simultaneous germline and somatic mutation analyses among individuals without leukemogenic point mutations (LPM), which we term CH-LPMneg. We quantify CH by estimating the total mutation burden. Because estimating somatic mutation burden without a paired-tissue sample is challenging, we develop a novel statistical method, the Genomic and Epigenomic informed Mutation (GEM) rate, that uses external genomic and epigenomic data sources to distinguish artifactual signals from true somatic mutations. We perform a genome-wide association study of GEM to discover the germline determinants of CH-LPMneg. We identify seven genes associated with CH-LPMneg (TCL1A, TERT, SMC4, NRIP1, PRDM16, MSRA, SCARB1).Functional analyses of SMC4 and NRIP1 implicated altered hematopoietic stem cell self-renewal and proliferation as the primary mediator of mutation burden in blood. We then perform comprehensive multi-tissue transcriptomic analyses, finding that the expression levels of 404 genes are associated with GEM. Finally, we perform phenotypic association meta-analyses across four cohorts, finding that GEM is associated with increased white blood cell count, but is not significantly associated with incident stroke or coronary disease events. Overall, we develop GEM for quantifying mutation burden from WGS and use GEM to discover the genetic, genomic, and phenotypic correlates of CH-LPMneg.
    DOI:  https://doi.org/10.1038/s41467-025-64236-x
  7. Blood. 2025 Oct 17. pii: blood.2025029010. [Epub ahead of print]
      Acute myeloid leukemia (AML) is a polyclonal malignancy marked by high relapse rates despite initial morphologic remission. Although measurable residual disease (MRD) is an established prognostic tool, increasing evidence supports a role for pre-emptive, MRD-directed therapy. AML monitoring is hampered by absence of a universal MRD marker, necessitating a more personalized approach. NPM1 is suited to an MRD-directed strategy as the mutation is AML-defining and monitoring methods highly sensitive. Critically, rising NPM1mut levels portend clinical relapse with high fidelity and recent studies demonstrate that venetoclax-based regimens induce rapid and deep MRD responses in a high proportion of patients with NPM1mut MRD relapse. The range of MRD-directed treatment options are expanding and include FLT3 and menin inhibitors for MRD relapse driven by FLT3-ITD and KMT2A rearrangements, respectively. To overcome the logistical issue of multiple MRD markers and associated therapies, we have developed a multi-target, multi-arm platform trial named INTERCEPT. Novel features include the potential to adaptively expand the range of MRD markers and directed therapies, seamless transition of patients from a local to centralized MRD monitoring framework, a clinical decision rules approach to allocate treatment in a hierarchical and pre-specified manner, creation of parallel protocol appendices to enable multiple industry partners to co-exist with commercial independence, and development of approaches to minimize the "MRD relapse to treatment" time interval. The future success of MRD-directed therapy will depend on rapid diagnostic turnaround, coordinated logistics and innovative clinical trial designs able to keep pace with advances in MRD-detection technologies and associated targeted therapies.
    DOI:  https://doi.org/10.1182/blood.2025029010
  8. J Clin Oncol. 2025 Oct 13. 101200JCO2501841
    PETHEMA group
       BACKGROUND: Quizartinib, an oral, selective, second-generation, type-II FMS-like tyrosine kinase 3 (FLT3) inhibitor with high binding affinity to internal tandem duplication (ITD) and wild-type FLT3, has shown early clinical activity as monotherapy in patients with relapsed/refractory FLT3-ITD-negative acute myeloid leukemia (AML). The phase 3 QuANTUM-First trial showed that quizartinib significantly prolonged survival vs placebo when added to standard chemotherapy, followed by single-agent maintenance, in patients with newly diagnosed (ND) FLT3-ITD-positive AML. We investigated the safety and efficacy of quizartinib in patients with ND FLT3-ITD-negative AML.
    METHODS: The phase 2, randomized, double-blind, placebo-controlled QUIWI trial enrolled patients aged 18-70 years with ND FLT3-ITD-negative (mutant-to-wild-type allelic ratio <0.03) AML. Patients were randomized 2:1 to receive standard induction and consolidation chemotherapy combined with either quizartinib 60 mg daily or placebo, followed by single-agent maintenance with quizartinib or placebo. The primary endpoint was event-free survival (EFS). Secondary endpoints included overall survival (OS) and safety.
    RESULTS: Overall, 273 patients were randomized to quizartinib (n=180) or placebo (n=93). At data cutoff, median EFS was 20.4 months and 9.9 months in the quizartinib and placebo arms, respectively (P=0.046). Median OS was not reached and 29.3 months in the quizartinib and placebo arms, respectively (P=0.012); three-year OS rates were 60.8% and 45.7%. The most frequently reported adverse events (any grade) were fever, rash, diarrhea, and mucositis.
    CONCLUSIONS: The addition of quizartinib to standard chemotherapy was associated with significantly longer EFS and OS than placebo in patients with ND FLT3-ITD-negative AML. ClinicalTrials.gov NCT04107727.
    DOI:  https://doi.org/10.1200/JCO-25-01841
  9. Blood. 2025 Oct 16. pii: blood.2025030741. [Epub ahead of print]
      Clinical trial eligibility criteria select a target population and reduce anticipated risks for participants but may unnecessarily limit participation both overall and differently across demographic groups. We previously abstracted eligibility criteria for 190 phase II/III acute myeloid leukemia (AML) trials and used Food and Drug Administration and professional society guidance on modernizing criteria to develop alternative, safety-based eligibility criteria for each trial. In this analysis, these trial- and safety-based eligibility criteria sets were applied to a retrospective cohort of 2226 newly-diagnosed patients across 8 hospitals to assess impacts on eligibility. Eligibility proportions increased from a median of 47.9% with trial-based criteria to 84.2% with safety-based criteria (median difference 30.0%; p<0.001); excluding age criteria, the increase was 11.5% (p<0.001). Non-Hispanic (NH)-Asian, NH-Black, NH-White, and Hispanic patients were eligible for median proportions of 41.1%, 44.0%, 47.9%, and 50.0% with trial-based criteria, increasing by 27.9-31.6% when using safety-based criteria (within group changes all p<0.001; between-group changes all p>0.05). Excluding age criteria, increases were between 10.0-11.9%. Moving from trial- to safety-based criteria decreased the proportion of trials with significant eligibility differences between NH-White and NH-Asian (-11.1%), NH-Black (-4.2%), and Hispanic (-12.1%) patients. Criteria significantly associated with increased eligibility and decreased between-group differences in eligibility were coronary artery disease, congestive heart failure, aspartate transaminase level, upper age limits, and prior malignancy. These data suggest that modernization of eligibility for AML trials to focus on safety-based criteria can improve both overall enrollment and population representation.
    DOI:  https://doi.org/10.1182/blood.2025030741
  10. Blood. 2025 Oct 17. pii: blood.2024027904. [Epub ahead of print]
      The European LeukemiaNet has periodically issued guidelines for the diagnosis and management of acute myeloid leukemia (AML) in adults. These consensus recommendations, most recently updated in 2022, incorporate recent advances in genomic testing, disease detection methods, target identification, and response assessment. Whilst similarities exist between AML in children and adults, pediatric AML is frequently characterized by unique cytogenetic and molecular features, which require distinct genetic and immunophenotypic diagnostics, therapeutic approaches, response assessment criteria, and supportive care strategies. To address these specific needs, an international panel of pediatric hematologist-oncologists, biologists, geneticists, and laboratory medicine scientists convened to develop recommendations for the diagnosis and management of AML in children, adolescents, and young adults (hereafter termed pediatric AML) that are discussed in this special report.
    DOI:  https://doi.org/10.1182/blood.2024027904
  11. Sci Adv. 2025 Oct 17. 11(42): eadx8662
      Acute myeloid leukemia (AML) is the most prevalent and deadliest adult leukemia. Its frontline treatment uses the BH3 mimetic venetoclax to trigger mitochondria-dependent apoptosis. However, drug resistance nearly always develops, calling for therapies to circumvent it. Advanced microscopy and genome-wide CRISPRi screen analyses pinpointed mitochondrial adaptations primarily mediated by the master regulator of cristae shape optic atrophy 1 (OPA1) as critical for BH3 mimetics resistance. Resistant AML cells up-regulate OPA1 to modify their mitochondrial structure and evade apoptosis. MYLS22 and Opitor-0, two specific and nontoxic OPA1 inhibitors, promote apoptotic cristae remodeling and cytochrome c release, synergizing with venetoclax in AML cells and xenografts derived from AML patients ex vivo and in vivo. Mechanistically, OPA1 loss renders AML cells dependent on glutamine and sensitizes them to ferroptosis by activating ATF4-regulated integrated stress responses. Overall, our data clarify how OPA1 up-regulation allows AML cells' metabolic flexibility and survival and nominates specific OPA1 inhibitors as efficacious tools to overcome venetoclax resistance in leukemia.
    DOI:  https://doi.org/10.1126/sciadv.adx8662
  12. EMBO Rep. 2025 Oct 16.
      Covalent inhibitors are an attractive targeting strategy that has expanded the development of degraders to target poorly druggable proteins including the E3 ligase RNF4. We show that RNF4 is a potential vulnerability of AML. High RNF4 expression levels correlate with poor patient survival and depletion of RNF4 results in increased sensitivity of AML cells to antileukemic drugs. Therefore, we aimed to develop chemical degraders (PROTACs) of RNF4 using a known covalent RNF4 ligand (CCW16), containing a chloro-N-acetamide group, as well as established E3 ligands targeting CRBN or VHL. However, while CCW16 and CCW16-derived PROTACs react potently with cysteines in recombinant RNF4, in cells, CCW16 forms covalent bonds with a large number of proteins, including peroxiredoxins. Consequently, CCW16 based PROTACs do not trigger degradation of RNF4, but induce the ferroptosis marker heme oxygenase-1 and impair cell viability in a distinct, RNF4-independent, ferroptotic cell death pathway. We hypothesize that other chloro-N-acetamide-containing E3 ligase ligands would also induce ferroptosis. Indeed, the RNF114 ligand EN219 also strongly induces ferroptosis, suggesting that ligands harboring this electrophile induce undesired off-target toxicity.
    Keywords:  AML; CCW16; Covalent PROTACs; Ferroptosis; RNF4
    DOI:  https://doi.org/10.1038/s44319-025-00593-4
  13. J Clin Oncol. 2025 Oct 15. JCO2500809
      Approximately 30%-50% of patients develop acute graft-versus-host disease (aGVHD) after allogeneic hematopoietic cell transplantation (Allo-HCT), representing a major limitation of this treatment. Although corticosteroids remain the standard first-line therapy for aGVHD, up to 50% of patients become steroid-refractory (SR). REACH2 is a phase III study of ruxolitinib versus best available therapy (BAT) in patients age 12 years and older with SR-aGVHD after Allo-HCT. We present the final efficacy and safety outcomes from REACH2 after 24 months of treatment. Cumulative median (range) duration of response was 167 (22-677) days with ruxolitinib and 106 (10-526) days with BAT. Median overall survival and event-free survival were 10.7 and 8.3 months for ruxolitinib, compared with 5.8 and 4.2 months, respectively, with BAT. Median failure-free survival was significantly longer with ruxolitinib than with BAT (4.86 v 1.02 months, P < .001). Similar numbers of nonrelapse mortality events were observed with ruxolitinib and BAT (72 v 71), and malignancy relapse/progression events remained low across both groups. Numerically higher chronic GVHD rates were noted with ruxolitinib than with BAT from 12 months; however, 95% confidence intervals overlapped. Safety observations were consistent with the primary analysis results. Ruxolitinib provided efficacy advantages over BAT in patients with SR-aGVHD over 24 months.
    DOI:  https://doi.org/10.1200/JCO-25-00809
  14. Haematologica. 2025 Oct 16.
      We studied 130 consecutive subjects who presented with (n = 29) or transformed to (n = 101) accelerated phase chronic myeloid leukemia (CML) and who received olverembatinib. 62 were in 2nd chronic phase. All failed ≥ 1 tyrosine kinase-inhibitors (TKIs) and 91 had BCR::ABL1T315I. Median follow-up was 28 months (InterQuartile Range, 10-74 months). The 6-year cumulative incidences of major cytogenetic response (MCyR), complete cytogenetic response (CCyR), major molecular response (MMR) and molecular response 4.0 (MR4.0) were 59% (95% Confidence Interval [CI] (49, 69%), 53% (42, 62%), 52% (41, 62%) and 42% (31, 53%), respectively. The 6-year probabilities of transformation-free survival (TFS), CML-related survival and survival were 81% (72, 90%), 76% (67, 87%) and 71% (61, 82%), respectively. In multi-variable analyses, an interval from diagnosis of CML to olverembatinib start < 29 months, failure to achieve complete hematologic response (CHR) on prior TKI therapy, hemoglobin concentration < 98 g/L, blood and/or bone marrow blasts ≥ 8%, and/or high-risk additional chromosome abnormalities at the start of olverembatinib therapy, as well as not achieving early MCyR on olverembatinib correlated with worse outcomes. RUNX1 and STAT5A variants were significantly associated with worse TFS in the 82 subjects with targeted DNA sequencing data. There were acceptable treatment-related adverse events. We conclude olverembatinib is effective and tolerable in subjects in accelerated phase CML failing prior TKI therapy.
    DOI:  https://doi.org/10.3324/haematol.2025.288249
  15. Ann Hematol. 2025 Oct 14.
      Acute myeloid leukemia (AML) is an aggressive and heterogenous malignancy, with unsatisfactory clinical outcomes even with very intensive treatment strategies. Previous research has revealed that Prader-Willi/Angelman syndrome 1 (NIPA1) is highly expressed in patients with AML and is negatively correlated with overall survival. However, studies on the molecular mechanism of NIPA1 in AML remain limited. To explore the role of NIPA1and its molecular mechanism in AML, we discovered through cellular experiments that NIPA1 was upregulated in M2 macrophages. NIPA1 knockdown inhibited M2 macrophage polarization and the survival of AML cells. In animal experiments, we also found that NIPA1 depletion restricted tumor growth in mice with AML. Further studies indicated that NIPA1 knockdown inhibited IGFBP2/epidermal growth factor receptor (EGFR) signaling in M2 macrophages, thereby weakening leukemia cell survival and reducing anthracycline resistance. Using both parental HL-60 and an adriamycin-resistant (HL-60/ADR) model, we show that TAM-targeted NIPA1 depletion enhances chemosensitivity and attenuates AML progression. Thus, NIPA1 could be used as a potential therapeutic strategy for immunotherapy in acute myeloid leukemia (AML).
    Keywords:  Acute myeloid leukemia; EGFR; IGFBP2; Macrophages; NIPA1
    DOI:  https://doi.org/10.1007/s00277-025-06688-1
  16. JAMA Cardiol. 2025 Oct 15.
       Importance: Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with increased risk of cardiovascular disease (CVD) events and mortality. However, there are no approved therapies for preventing or treating CHIP.
    Objective: To investigate whether low-dose aspirin might benefit older adults with CHIP for the primary prevention of CVD.
    Design, Setting, and Participants: This was a prespecified substudy of the Aspirin in Reducing Events in the Elderly (ASPREE) double-blind, randomized clinical trial of daily low-dose aspirin vs placebo evaluating disability-free survival, which took place at primary and community care facilities in the US and Australia. Enrollment was from March 2010 to December 2014, and the randomized trial ended in June 2017. Community-dwelling Australian adults aged 70 years and older without a diagnosed cardiovascular event, atrial fibrillation, a serious intercurrent illness likely to cause death within the next 5 years, anemia, or a current or recurrent condition with a high risk of bleeding were included in the original study. Of 19 114 in the original trial, 11 402 were included in the substudy, and 9434 were included in the analysis. Follow-up for this substudy went through June 2022, with data analysis in February 2025. In-trial median (IQR) follow-up time was 4.6 (3.5-5.6) years, and posttrial observational follow-up was 8.7 (7.5-10.1) years from randomization.
    Interventions: Participants were randomized to aspirin, 100 mg, daily or placebo.
    Main Outcomes and Measures: CHIP was measured in blood specimens collected at trial entry. Major adverse cardiovascular events (MACEs), including fatal and nonfatal ischemic stroke, nonfatal myocardial infarction and coronary heart disease death, and clinically significant bleeding were adjudicated by independent expert committees blinded to trial-group assignments.
    Results: A total of 9434 participants (median [IQR] age, 73.7 [71.6-77.1] years; 5067 [54%] female) provided a sample at baseline for analysis, 2124 of whom (23%) had CHIP at variant allele fraction (VAF) ≥2%, with 532 (5.6%) at ≥10% VAF. CHIP was not associated with increased risk of MACEs at 2% to 10% VAF (adjusted hazard ratio [aHR], 0.84, 95% CI, 0.68-1.03; P = .09) or ≥10% VAF (aHR, 0.80, 95% CI, 0.57-1.12; P = .19). However, CHIP was associated with increased risk of clinically significant bleeding (2%-10% VAF: aHR, 1.24; 95% CI 1.02-1.51; P = .03; ≥10% VAF: aHR, 1.21; 95% CI, 0.85-1.73; P = .28). There was no evidence of a differential effect of aspirin according to presence of CHIP on MACEs (without CHIP: HR, 0.91; 95% CI, 0.72-1.16; 2%-10% VAF: HR, 1.40; 95% CI, 0.77-2.53; ≥10% VAF: HR, 1.33; 95% CI, 0.52-3.37; heterogeneity P = .35) or clinically significant bleeding (without CHIP: HR, 1.64; 95% CI, 1.22-2.30; 2%-10% VAF: HR, 1.45; 95% CI, 0.82-2.57; ≥10% VAF: HR, 1.41; 95% CI, 0.49-4.07; heterogeneity P = .91).
    Conclusion and Relevance: In this secondary analysis of a randomized clinical trial of daily low-dose aspirin in healthy adults 70 years and older, CHIP was not associated with higher CVD risk. However, participants with CHIP had a greater risk of clinically significant bleeding. There was no evidence that participants with CHIP were more likely than those without CHIP to benefit or experience more harm from aspirin when used for primary prevention of CVD events.
    Trial Registration: ClinicalTrials.gov Identifier: NCT01038583.
    DOI:  https://doi.org/10.1001/jamacardio.2025.3756
  17. Blood. 2025 Oct 16. pii: blood.2025028643. [Epub ahead of print]
      The peptide hepcidin is produced by the liver and serves as the central negative regulator of iron trafficking. Recently, drugs that affect the hepcidin pathway have been evaluated as potential treatment options for both controlling the degree of erythrocytosis in polycythemia vera (PV) patients as well as correcting anemia associated with myelofibrosis (MF). Under normal conditions, increased hepcidin levels limit iron absorption from the gastrointestinal tract and iron recycling from liver and splenic macrophages, thus decreasing plasma iron levels and restricting iron availability for erythropoiesis. In PV, however, unrestricted erythropoiesis occurs despite low systemic iron levels. Since hepcidin levels are relatively low in PV patients, hepcidin agonists (rusfertide, divesiran, sapablursen) are undergoing clinical development to control PV associated erythrocytosis, thereby reducing the need for therapeutic phlebotomies and myelosuppressive therapeutic options. By contrast, hepcidin levels are increased in MF patients leading to the trapping of iron in tissue macrophages which creates a picture which resembles the anemia of chronic inflammation. A number of strategies to lower hepcidin levels (the JAK2 inhibitors pacritinib and momelotinib, anti-hemojuvelin monoclonal antibody DISC-0974C) are currently undergoing clinical development to make systemic iron available for erythropoiesis and alleviate the degree of MF associated anemia. These new therapeutic options that modulate iron trafficking in PV and MF patients represent the application of greater knowledge of iron trafficking to create novel therapeutic options to treat patients with hematological malignancies.
    DOI:  https://doi.org/10.1182/blood.2025028643
  18. Mol Oncol. 2025 Oct 17.
      CDK11 is a cyclin-dependent kinase with a role in transcription and RNA splicing and represents a potential target for cancer treatment. We show that blocking CDK11 activity with the OTS964 inhibitor causes p53 stabilisation through MDM2 downregulation. Under these conditions, p53 activates the expression of its downstream effector CDKN1A (p21WAF1), produced in two isoforms, the canonical p21C and the recently described p21L. We compared the ability of both isoforms to block proliferation and showed that p21L partially lost its inhibitory potential, likely due to the missing cyclin-binding Cy2 and PCNA-interacting motifs and its cytoplasmic localisation. We identified the epitopes of four p21WAF1 antibodies using phage display to determine isoform specificity. Moreover, we show that the trigger for p21L induction is inhibition of the spliceosomal protein SF3B1. CDK11 activates SF3B1 by phosphorylation, and inhibition of either SF3B1 or CDK11 induces p21L. We discovered an isoform similar to human p21L in murine cells, suggesting evolutionary conservation of CDKN1A alternative splicing. Our results uncover an unknown link between RNA splicing and proliferation control involving a novel isoform of a key cell cycle inhibitor.
    Keywords:  MDM2; SF3B1; cyclin‐dependent kinase 11; p21L; p21WAF1; p53
    DOI:  https://doi.org/10.1002/1878-0261.70143