bims-tremyl Biomed News
on Therapy resistance biology in myeloid leukemia
Issue of 2026–06–14
25 papers selected by
Paolo Gallipoli, Barts Cancer Institute, Queen Mary University of London



  1. J Clin Oncol. 2026 Jun 11. 101200JCO2601159
       PURPOSE: Revumenib is an oral inhibitor of menin-KMT2A, a key dependency in acute myeloid leukemia (AML) with KMT2A rearrangement (KMT2Ar), NPM1 mutation (NPM1mt), or NUP98 rearrangement (NUP98r). Preclinical studies suggest synergy with BCL2 inhibition.
    PATIENTS AND METHODS: In this phase 1-2 study, we evaluated an all-oral regimen of revumenib, decitabine/cedazuridine, and venetoclax in patients ≥12 years of age with relapsed or refractory AML. Decitabine/cedazuridine was given days 1-5, venetoclax days 1-14, and revumenib twice daily days 1-28. The primary objectives were to determine the recommended phase 2 dose (RP2D) and to assess efficacy according to the composite complete remission (CRc) rate.
    RESULTS: Forty-two patients were enrolled (median age, 40 years; range, 12-82) including 40% with KMT2Ar, 38% with NPM1mt, and 21% with NUP98r. Patients had a median of 2 prior lines of therapy; 52% had prior venetoclax. The RP2D of revumenib was 160 mg twice daily with a strong CYP3A4 inhibitor.Grade ≥3 adverse events included febrile neutropenia (36%), lung infection (21%), and thrombocytopenia (21%). Differentiation syndrome occurred in 10% (5% grade 3) and resolved with glucocorticoids.The CRc rate was 71%, and the CR or complete remission with partial hematologic recovery (CR/CRh) rate was 60%, with measurable residual disease negativity by flow cytometry in 80% of these patients. The median duration of CR/CRh for all patients was 10.5 months, not reached in KMT2Ar, 10.7 months in NPM1mt, and 5.9 months in NUP98r. Emergent mutations in the menin-binding site occurred in 13%.
    CONCLUSION: This combination was associated with high response rates and durable remissions, with an acceptable safety, in heavily pretreated patients with AML harboring alterations susceptible to menin inhibition.
    Keywords:  AML; KMT2A; NPM1; NUP98; menin
    DOI:  https://doi.org/10.1200/JCO-26-01159
  2. Blood. 2026 Jun 08. pii: blood.2026033576. [Epub ahead of print]
      NPM1-mutated acute myeloid leukemia (AML) is genetically well-defined, but clinical outcomes remain heterogeneous, suggesting that quantitative clonal features may refine current risk stratification. We analyzed 688 intensively treated NPM1-mutated AML integrating variant allele frequency (VAF), mutation order, and clonal architecture inferred by PyClone and ClonEvol. Co-mutations were present in 97% of patients (median = 3 per case), dominated by DNMT3A (49%), FLT3-ITD (46%), TET2 (22%), and IDH2 (20%). Prognostic modelling of NPM1 VAF identified an optimal cut-off of 31.44%, defining NPM1high and NPM1low groups. NPM1low correlated with splicing-related alterations and independently predicted inferior overall (HR = 1.46; p = 0.037) and relapse-free survival (HR = 1.40; p = 0.036). Gene-specific VAF analyses revealed divergent effects across partners, high DNMT3A, FLT3-OTHER, KRAS, and PTPN11 burdens were adverse, whereas high IDH2 VAF was protective. Combined models showed that patients with NPM1high and favorable co-mutation VAFs had the best outcomes, while dual unfavorable burdens conferred the poorest survival. Mutation ordering inferred from VAFs positioned NPM1 after epigenetic and splicing lesions but before signaling and transcription-factor mutations. Non-canonical orders, such as early FLT3-OTHER/TKD or WT1 prior to NPM1, significantly stratified outcomes. Clonal reconstruction revealed predominantly linear evolutionary trajectories (84.3%), with increased mutational burden and clonal diversity associating with inferior survival. Notably, intra-clonal co-localization of NPM1 with IDH1 or TET2 was associated with improved outcomes, whereas co-localization with WT1 predicted dismal prognosis. These results demonstrate that quantitative and structural dimensions of clonality refine the biological and prognostic landscape of NPM1-mutated AML beyond mutational status alone.
    DOI:  https://doi.org/10.1182/blood.2026033576
  3. Nat Commun. 2026 Jun 11.
      Acute myeloid leukemia (AML) is a prevalent hematologic malignancy. Mutations in Nucleophosmin (NPM1c) is the most frequent genetic alterations in AML. However, the epigenetic regulatory mechanisms of this AML subtype remain unclear. The cohesin complex, regulated by the acetyltransferase ESCO2, orchestrates chromatin organization and regulates gene expression. Here, we show that loss of ESCO2 promotes the progression of NPM1-mutated AML by destabilizing cohesin and the NuRD complex on chromatin, thereby enhancing the expression of genes associated with leukemia self-renewal capacity. Pharmacological HDAC8 inhibition restores SMC3 binding and induces differentiation and apoptosis in NPM1-mutated AML cells. Simultaneously targeting HDAC8 and nuclear exporter XPO1 reverses aberrant epigenetic landscape and represses self-renewal gene expression induced by ESCO2 deficiency. The combined treatment effectively eliminates NPM1-mutated AML cell lines and primary human AML cells in vitro and in vivo. This study reveals an ESCO2 deficiency-induced aberrant epigenetic landscape via SMC3 hypoacetylation and identifies a potential therapeutic strategy for NPM1-mutated AML.
    DOI:  https://doi.org/10.1038/s41467-026-74343-y
  4. Nucleic Acids Res. 2026 Jun 08. pii: gkag529. [Epub ahead of print]54(11):
      Loss-of-function mutations in BCOR, a subunit of the non-canonical Polycomb Repressive Complex 1.1 (PRC1.1), are frequently observed in acute myeloid leukemia (AML) and associate with adverse risk. Paradoxically, leukemic stem cell viability in BCOR wild-type AMLs strongly depends on PRC1.1 activity. Here, we use BCOR and KDM2B degron models to study PRC1.1 dependency in leukemic cells and find that BCOR is a bridging factor tethering the catalytic and chromatin-binding moieties of the PRC1.1 complex. BCOR degradation induces a quick localized loss of H2AK119ub at PRC1.1 target genes, whereas PRC2-induced H3K27me3 remains unaffected. Degron-mediated depletion of BCOR or KDM2B induces a rapid but time-dependent transcriptional induction, whereby late-upregulated genes are more heavily decorated with H3K27me3 compared to early-upregulated genes. Combined PRC1.1 inactivation and PRC2 inhibition further amplifies gene induction, suggesting collaborative yet distinct control over target genes. Strikingly, both JARID2/AEBP2 and SUZ12 knockout cells, devoid of PRC2.2 or PRC2.1/PRC2.2 respectively, retain PRC1.1 loss-induced transcriptional activation, underscoring that PRC1.1 can repress target genes independently of a downstream PRC2.2-canonical PRC1 repressive axis. Finally, combined targeting of PRC1.1 and PRC2 induces differentiation of leukemic cells, emphasizing that co-targeting PRC1.1 and PRC2 represents a promising strategy to improve treatment of AML patients.
    DOI:  https://doi.org/10.1093/nar/gkag529
  5. J Clin Invest. 2026 Jun 09. pii: e204429. [Epub ahead of print]
      Clonal hematopoiesis (CH) is the age-related expansion of mutated hematopoietic stem cells without hematologic abnormalities. In patients with solid tumors, CH is associated with higher mortality and may evolve to therapy-related myeloid neoplasms; however, the mechanisms by which cancer treatments promote CH dynamics remain largely unknown. Here, we analyzed 392 serial samples from a prospective cohort of breast cancer patients and showed that cytotoxic treatments led to strong therapeutic bottlenecks, resulting in significant reductions in hematopoietic allelic populations and differential clonal selection. Positively selected CH that expanded through dose-dependent therapeutic bottlenecks harbored mutations in TP53, PPM1D, SRCAP, DNMT3A, and YLPM1. Patients with positively selected CH during treatment had the shortest progression-free and overall survival compared to patients with unchanging or negatively selected CH across all therapies. These findings, validated in independent breast cancer and pan-cancer cohorts, provide strong evidence for clinical relevance of monitoring CH during cancer treatment.
    Keywords:  Breast cancer; Clinical Research; Clonal selection; Genetics; Hematopoietic stem cells; Oncology
    DOI:  https://doi.org/10.1172/JCI204429
  6. bioRxiv. 2026 Jun 03. pii: 2026.05.31.729063. [Epub ahead of print]
      The JAK2 V617F (JAK2 VF ) driver mutation is found in 95% of patients with polycythemia vera (PV), a progressive myeloproliferative neoplasm. Current treatments suppress excessive hematopoiesis but lack specificity for targeting JAK2 VF cells, are unable to deplete mutant stem/progenitor cells and ultimately result in drug resistance. We discovered that the FDA-approved antibiotic, linezolid (LZD), ameliorates the PV phenotype across multiple model systems. LZD suppressed cell proliferation and STAT5 signaling, altered the cell cycle, and increased apoptosis of JAK2 VF -harboring human erythroleukemia cells, but not in wild-type acute leukemia cells. Computational modelling indicated that LZD interacts specifically with mutant JAK2 VF but not with wild-type JAK2 protein. We further showed that, in JAK2 VF mice that faithfully recapitulate human PV, LZD mitigates disease burden by selectively targeting JAK2 VF stem cells thereby normalizing spleen size and blood counts. LZD also inhibited hematopoietic colony formation by patient-derived peripheral blood mononuclear cells, with the more primitive progenitors being preferred targets. Importantly, LZD selectively decreased JAK2 VF+ colony numbers, without impacting wild-type JAK2 colonies. In all, the data provide a firm foundation for evaluating LZD-like molecules as an effective therapy for PV and other myeloproliferative neoplasms.
    Key points: Linezolid acts as a JAK2 V617F IZselective inhibitor in PV mouse models and PV patient samples while sparing wildIZtype hematopoiesis. Linezolid acts directly on JAK2 V617F hematopoietic stem cells.
    DOI:  https://doi.org/10.64898/2026.05.31.729063
  7. Hemasphere. 2026 May;10(5): e70379
      Myelodysplastic syndromes (MDS) are heterogenous disorders in which response assessment remains challenging. In acute myeloid leukemia (AML), measurable residual disease (MRD) by multiparametric flow cytometry (MFC) is prognostic and guides decision-making after two cycles of intensive chemotherapy, but its role in high-risk MDS (hrMDS) is unknown. We aimed to determine the prognostic impact of MFC-MRD (0.1% cutoff) for overall survival (OS) and the cumulative incidence of relapse (CIR) in intensively treated hrMDS. After stringent selection from 3269 patients enrolled in prior HOVON-SAKK MDS/AML trials, we identified 91 ICC 2022-defined hrMDS patients with available MFC-MRD. MFC-MRD positivity was detected in 24% and associated with inferior survival (5-year OS: 22.7% vs. 43.7%; P = 0.010) and higher relapse risk (5-year CIR: 72.7% vs. 47.2%; P = 0.014). In multivariable analyses stratified by trial and adjusted for, among others, the presence of a biallelic TP53 mutation, MFC-MRD positivity remained associated with poorer OS (hazard ratio (HR) 2.12 [95% CI 1.15-3.90]; P = 0.017) and increased CIR (subdistribution HR 2.15 [95% CI 1.11-4.14]; P = 0.022). To account for the potential confounding effect of allogeneic hematopoietic stem cell transplantation, additional sensitivity analyses were performed and confirmed that MRD positivity remained significantly associated with inferior survival outcomes. Lastly, an exploratory cross-disease comparison showed that MRD-negative (MRDneg) hrMDS patients had similar survival outcomes to MRD-positive (MRDpos) AML patients. These findings demonstrate the prognostic value of MFC-MRD in intensively treated hrMDS and provide rationale for prospective trials of MRD-informed transplant and post-remission strategies.
    DOI:  https://doi.org/10.1002/hem3.70379
  8. Stem Cell Reports. 2026 Jun 11. pii: S2213-6711(26)00170-0. [Epub ahead of print] 102959
      Platelet-biased hematopoietic stem cells (PLT-HSCs) play key roles in normal physiology, aging, and blood cancer. However, currently, no markers allow their accurate identification or prospective isolation. We here combine single-mouse hematopoietic stem cell (HSC) gene expression, chromatin accessibility, and surface proteome profiling to identify subtype-specific markers. Using machine learning, we identified markers (CD61hiCD274hiCD357loCD27lo) that isolate PLT-HSCs to high purity, validated by single-cell transplantation. Furthermore, we develop a minimal expression marker panel that discriminates PLT- and multi-lineage (MUL-)HSCs using microfluidics-based single-cell RT-qPCR. We show that both methods detect the age-associated increase in PLT-HSCs, while poly(I-C)-induced chronic inflammation did not alter HSC lineage bias. In contrast, romiplostim treatment increased MUL-HSC prevalence. Finally, using spectral flow cytometry to simultaneously quantify cell cycle and HSC lineage bias, we show that platelet depletion selectively activates PLT-HSCs. Together, these approaches allow accurate isolation of PLT-HSCs and robust quantification of lineage bias under perturbation.
    Keywords:  hematopoietic stem cells; lineage bias; platelet-biased HSCs; single-cell multiomics
    DOI:  https://doi.org/10.1016/j.stemcr.2026.102959
  9. Blood Adv. 2026 Jun 09. pii: bloodadvances.2026020264. [Epub ahead of print]
      Relapse is the predominant cause of treatment failure after allogeneic hematopoietic cell transplantation (allo-HCT) in FLT3-ITD-mutated AML. Although measurable residual disease (MRD) is increasingly used for risk stratification, optimal FLT3-ITD MRD assessment, the prognostic value of peri-transplant MRD dynamics, and their implications to transplant-related decision-making remain unclear. We conducted a multicenter retrospective study of 219 patients with FLT3-ITD-mutated AML in morphologic complete remission at transplantation, assessing peri-transplant MRD by PCR-next-generation sequencing (PCR-NGS). Pre-transplant MRD positivity (≥ 0.001% by PCR-NGS) was associated with inferior outcomes versus MRD negativity (2-year relapse-free survival [RFS], 56.8% vs. 86.5%; cumulative incidence of relapse [CIR], 30.0% vs. 6.9%; overall survival [OS], 65.9% vs. 88.4%; all p<0.001). Peri-transplant MRD dynamics outperformed single time-point assessments, identifying high-risk patients such as those with post-HCT MRD conversion. And post-HCT FLT3 inhibitor maintenance independently improved RFS (p = 0.003), with greatest benefit observed in MRD-positive patients. These findings support PCR-NGS-based molecular MRD assessment to refine risk stratification and guide individualized transplant strategies in FLT3-ITD-mutated AML.
    DOI:  https://doi.org/10.1182/bloodadvances.2026020264
  10. Blood Adv. 2026 Jun 12. pii: bloodadvances.2025018827. [Epub ahead of print]
      VEXAS syndrome is a clonal hemato-inflammatory disorder impacting older, predominantly male patients, characterized by systemic inflammation and progressive bone marrow failure. It is caused by somatic mutations in UBA1, an X-linked gene, essential for initiating cellular ubiquitination. Loss-of-function mutations, most commonly M41 missense variants, lead to decreased expression of the cytoplasmic isoform, UBA1b, resulting in accumulation of misfolded proteins and activation of the endoplasmic reticulum stress pathway. Patients classically present with systemic and often refractory inflammation, requiring chronic glucocorticoid treatment and targeted immunosuppressive therapies. A central hallmark of this syndrome is progressive bone marrow failure and associated cytopenia, with a diagnosis of myelodysplastic syndromes (MDS) being reported in approximately 30-50% of patients while only 1% of unselected MDS patients have UBA1 mutations. This review examines current literature on distinct MDS features reported in VEXAS syndrome. We first summarize the defects and alterations in the hematopoietic system from UBA1 mutations, including associated peripheral blood and bone marrow findings. Next, we describe the histological and molecular characteristics of patients with VEXAS syndrome, with and without MDS, and review potential treatment strategies, including responses to hypomethylating agents. Finally, we highlight that VEXAS-associated MDS is a challenging diagnosis but one with unique clinical, laboratory, and morphological features, including prognostic implications.
    DOI:  https://doi.org/10.1182/bloodadvances.2025018827
  11. Am J Hematol. 2026 Jun 08.
      Hypomethylating agents (HMA) and allogeneic hematopoietic stem cell transplantation (alloHSCT) have both demonstrated remissions in VEXAS; however, comparative data is lacking. We conducted a multicenter, retrospective analysis of 66 patients diagnosed with VEXAS syndrome treated with HMA (n = 35) or alloHSCT (n = 31). Baseline characteristics such as genetics, co-morbidities, and performance status were balanced between the groups, except older age in the HMA group. Median follow-up from therapy initiation was 18 months (95% CI: 11-26), and 14 (21%) deaths were reported (alloHSCT n = 3; HMA n = 11). Among all evaluable patients within the alloHSCT cohort, all patients achieved molecular remission, and a substantial proportion of patients discontinued glucocorticoids (58%). In contrast, HMA therapy was associated with lower but meaningful rates of molecular remission (22%) and glucocorticoid discontinuation (6%). In a real-world setting, HMA therapy was associated with a high discontinuation rate related to toxicity or lack of response. On multivariable analysis adjusted for age and Charlson Comorbidity Index, alloHSCT was associated with improved overall survival (HR = 0.20, 95% CI: 0.05-0.81; p = 0.024). This association remained consistent across multiple ancillary sensitivity analyses, including restriction to transplant-eligible patients, patients aged ≤ 75 years, 1:1 matching, and propensity score-based weighted analyses. Although limited by retrospective design, these findings suggest that alloHSCT remains an attractive and potentially curative strategy in selected patients with VEXAS. Prospective validation of these findings is warranted.
    Keywords:  HMA; UBA1; VEXAS; allogeneic transplantation; azacitidine; molecular remission; myelodysplastic syndrome
    DOI:  https://doi.org/10.1002/ajh.70401
  12. Nat Commun. 2026 Jun 10.
      Eradicating leukemic stem cells (LSCs), a major driver of primary resistance and relapse in chronic myeloid leukemia (CML) following tyrosine kinase inhibitor (TKI) treatment, is critical for achieving a cure. Previously, we identified that ANP32B promotes CML LSCs' survival and leukemogenesis by directly binding and inhibiting p53 activity, suggesting a therapeutic opportunity. Here, we show that 1-amino-8-naphthol-2,4-disulfonic acid (ANDS) binds unacetylated p53 and restores p53 activity by disrupting ANP32B-p53 interaction. Consequently, ANDS inhibits CML cell proliferation, impairs LSC function and prolongs survival in the CML mouse model while sparing normal progenitor cells. Based on notion that ANDS, as a previously-identified CaMKP inhibitor, potentially activates p-CaMKIIγ to accelerate CML progression, we find that ANDS combination with KN93, a p-CaMKIIγ inhibitor, synergistically suppresses both TKI-sensitive and -resistant CML. Thus, we highlight that ANDS alone or in combination with CaMKP inhibitor could become a therapeutic strategy for eradicating LSCs and overcoming TKI-resistance in CML.
    DOI:  https://doi.org/10.1038/s41467-026-73951-y
  13. Leukemia. 2026 Jun 09.
      In acute myeloid leukemia (AML), the insertion site of internal tandem duplications (ITDs) within the FLT3 gene critically determines the sensitivity to tyrosine kinase inhibitors (TKIs). Despite recent advances, patients harboring ITDs in the tyrosine kinase domain (TKD) still lack effective therapeutic options. To elucidate the molecular basis underlying the differential TKI sensitivity of FLT3-ITD cells, we integrated high-resolution mass spectrometry-based (phospho)proteomics with subcellular fractionation. Our analysis revealed that midostaurin induces the subcellular redistribution of approximately 2500 proteins involved in crucial biological processes, including cell cycle control, autophagy, and metabolism. Functional analyses further demonstrated that the ITD insertion site determines the autophagy response to midostaurin and modulates mitochondrial metabolism, influencing organelle architecture and ATP production, even at steady state. Importantly, by integrating subcellular proteomic dataset with functional metabolic assays, we uncovered a lipid-dependent vulnerability of FLT3-ITD cells: lipid restriction enhances FLT3 trafficking to the plasma membrane, and markedly reduces cell viability, restoring midostaurin sensitivity of resistant FLT3-ITD cells. Together, our findings reveal that the FLT3-ITD insertion site orchestrates a coordinated remodeling of subcellular protein organization, autophagy, and metabolism, and identify lipid-mediated control of FLT3 compartmentalization as a therapeutically actionable mechanism to overcome TKI resistance in FLT3-ITD AML.
    DOI:  https://doi.org/10.1038/s41375-026-03000-6
  14. Blood Adv. 2026 Jun 11. pii: bloodadvances.2026020255. [Epub ahead of print]
      Ruxolitinib is widely used in Polycythemia Vera (PV) following hydroxyurea failure. However, validated response criteria to predict long-term outcomes in ruxolitinib-treated patients are lacking, complicating clinical decision-making. We investigated predictors of event-free survival (EFS, including progression to post-PV myelofibrosis, thrombosis, hemorrhages, or death) after 6 months of ruxolitinib in 178 PV patients enrolled in the observational PV-ARC study (NCT06134102). After a median follow-up from ruxolitinib start of 3.50 years, 15 patients died, 7 had a thrombosis, 9 a hemorrhage, and 21 progressed to myelofibrosis. Overall, 5-year EFS was 70.4%. Leukocytosis (>10x109/L), thrombocytosis (>400x109/L), phlebotomy need, lack of spleen length reduction ≥50% (SR50) and ruxolitinib dose <10 mg BID at three timepoints (baseline, month 3 and 6), were tested for association with EFS. Multivariable analysis identified three independent risk factors: (1) ruxolitinib dose<10mg BID at ≥1 timepoint (HR 1.94, p=0.047), (2) no SR50 at months 3 and 6 (HR 2.65, p=0.009), (3) phlebotomy requirement at ≥2 timepoints (HR 2.11, p=0.039). Points were assigned as follows: 1 to phlebotomies at one timepoint; 2 to phlebotomies at ≥2 timepoints and to ruxolitinib <10 mg BID at ≥1 timepoint; 2.5 to lack of SR50. Based on cumulative scores, we developed the PV-Response to Ruxolitinib after 6 Months (PV-RR6) prognostic model, identifying three risk categories: low (score 0, 5-year EFS: 89.4%, n=63), intermediate (score 1-2.5, EFS: 71.0%, n=82), and high (score >2.5, EFS: 38.9%, n=33) (p<0.001). PV-RR6 enables early identification of patients at risk of poor outcomes, supporting timely treatment optimization in ruxolitinib-treated patients.
    DOI:  https://doi.org/10.1182/bloodadvances.2026020255
  15. Hemasphere. 2026 May;10(5): e70393
      Whether clonal hematopoiesis (CH) in follicular lymphoma (FL) patients affects clinical outcome or is merely a bystander phenomenon is unclear. We leveraged the Phase III Fondazione Italiana Linfomi FOLL12 trial, which treated patients with advanced-stage FL with R-CHOP or R-Bendamustine, to evaluate the role of myeloid CH at baseline and after chemoimmunotherapy (CIT). A total of 528 serial blood samples from 242 FL were analyzed by CAPP-Seq. At baseline, CH occurred in 35.5% patients with DNMT3A (N = 41, 16.9%) and TET2 (N = 29, 12.0%) being the most frequently mutated genes. After a median follow-up of 8.2 years, CH at baseline did not impact progression-free survival (PFS), overall survival (OS), or risk of transformation (P = 0.660, P = 0.230, and P = 0.584, respectively), but instead associated with therapy-related hematological toxicities driven by TET2 mutations. CH dynamics after the genotoxic pressure imposed by CIT was evaluated in 211 patients provided with sequential samples. CIT significantly expanded both prevalence and size of CH, with clones affected by DNA damage response (DDR) gene mutations exhibiting the highest fitness. Distinct selective pressures were observed between R-CHOP and R-Bendamustine, with the latter creating a tighter bottleneck that facilitates the emergence of fitter CH clones preferentially carrying TP53 mutations. Patients acquiring fit DDR clones (N = 37) had inferior long-term outcomes, including independent increased risk of second malignancies (hazard ratio [HR] 2.63, P = 0.035) that developed in 28 patients, and shorter OS (HR 3.28, P = 0.008). CH emerges as a novel and potentially valuable biomarker in FL, capable of predicting long-term toxicities that are key endpoints in indolent lymphoid malignancies characterized by long-lasting survival.
    DOI:  https://doi.org/10.1002/hem3.70393
  16. Nature. 2026 Jun 10.
      Clonal haematopoiesis (CH) activates inflammation and increases the risk of atherosclerosis1,2. Whether lifestyle alters CH clone expansion or the phenotypic programming of CH mutant cells, thereby affecting atherosclerosis, is unknown. Here, in humans and mice and across mutations in Jak2, Tet2, Trp53 and Dnmt3a, we demonstrate mutation-dependent responses to sleep and exercise in CH and show that mutant cells are uniquely sensitive to lifestyle. In two human datasets, moderate-to-vigorous physical activity was associated with lower prevalence of non-DNMT3A-driven CH. In atherogenic mice with Jak2V617F or Tet2 loss of function (LOF), but not Trp53 LOF or Dnmt3aR878H CH, uninterrupted sleep or exercise curtails clone expansion. In CH with the Jak2V617F mutation, sleep and exercise reduces clone expansion by selectively reprogramming mutant, but not cohabitant wild type, haematopoietic progenitor cells towards antiproliferative and metabolically healthy phenotypes by tempering bone marrow macrophage-haematopoietic progenitor cell IL-1β signalling. Sleep or exercise also lessens Jak2V617F-driven, Tet2 LOF-driven and Trp53 LOF-driven, but not Dnmt3aR878H-driven, atherosclerosis by locally reprogramming mutant vascular macrophages, independent of peripheral clone dynamics. In Jak2V617F, but not adjacent wild type, aortic macrophages, uninterrupted sleep blunts CLEC4E-dependent inflammasome activation, consequently diminishing lesions. Exercise, meanwhile, activates PAC1+ neurons in the locus coeruleus, raising the levels of peripheral noradrenaline, which signals through adrenergic receptor β2 (ADRβ2) whose expression is preserved by exercise in Jak2V617F, but not cohabitant wild type, aortic macrophages, selectively repressing their inflammatory programming and atherosclerosis. Our findings establish that healthy lifestyles gene-specifically diminish CH and selectively reprogram mutant haematopoietic progenitor cells and macrophages to maintain cardiovascular health.
    DOI:  https://doi.org/10.1038/s41586-026-10634-0
  17. Blood Adv. 2026 Jun 11. pii: bloodadvances.2026019701. [Epub ahead of print]
      Among patients with chronic myeloid leukemia (CML) aiming for tyrosine kinase inhibitor (TKI) discontinuation, second-generation TKIs (2G-TKIs) are used as one of the first-line options because they induce faster and deeper molecular responses than imatinib. However, predictors of attaining and sustaining MR4.5 (BCR::ABL1 International Scale [IS] ≤ 0.0032%) during 2G-TKI therapy remain undefined. We analyzed 431 patients enrolled in the phase III Japan Adult Leukemia Study Group (JALSG) CML212 trial, comparing nilotinib at 300 mg twice daily (n = 218) and dasatinib at 100 mg once daily (n = 213) as first-line therapy. The objective was to identify predictors of MR4.5 attainment and TKI discontinuation eligibility (TDE). Candidate variables assessed within 6 months included the EUTOS long-term survival (ELTS) score; BCR::ABL1 IS at baseline, 3 months, and 6 months; and IS-derived halving times, HT(0-3) and HT(3-6). TDE was defined as ≥3 years of TKI therapy with ≥2 consecutive years of sustained MR4.5. With a median follow-up of 3.0 years, the cumulative incidence of MR4.5 was 46.6%, and 36.3% of patients achieving MR4.5 met TDE criteria. In multivariable models, HT(0-3) (subdistribution hazard ratio [HR], 2.23; 95% CI, 1.09-4.55) and the 6-month IS (HR, 0.38; 95% CI, 0.31-0.47) were independent predictors of MR4.5 attainment, whereas only the 6-month IS predicted TDE (odds ratio, 0.37; 95% CI, 0.24-0.56). This study demonstrates that molecular response at 6 months after TKI initiation has important clinical value in early stratification of MR4.5 attainment and TDE in patients receiving 2G-TKI therapy.
    DOI:  https://doi.org/10.1182/bloodadvances.2026019701
  18. Nat Cancer. 2026 Jun 12.
    Clinical Proteomic Tumor Analysis Consortium
      Acute myeloid leukemia (AML) is a genetically and phenotypically heterogeneous hematological malignancy. Here, to better define this clinically taxing and translationally challenging malignancy, we applied a multiomics approach, consisting of 13 modalities to analyze 173 treatment-naive individuals with AML. By integrating these 'omes', we identified distinct AML subtypes, genotype-phenotype associations, biomarkers and pathobiological mechanisms. Across the spectrum of primitive and committed AML, we found extensive metabolomic and lipidomic reprogramming driven by divergent MYC and mTOR activity. We linked metabolic changes to striking hyperacetylation of mitochondrial proteins in CEBPA-mutant AML. Protein-centric subtyping revealed a distinct NPM1-mutant subset characterized by outlier expression of FOXC1 and HOXB8/9. To nominate therapeutic targets across subtypes, we developed a multiomic machine-learning approach and validated MTA1 as a contributor to panobinostat resistance. Altogether our findings underscore the complex nature of AML and provide a clinically and translationally informed unified view that reveals coalescent phenotypes across multiomic layers.
    DOI:  https://doi.org/10.1038/s43018-026-01175-6
  19. Blood Adv. 2026 Jun 05. pii: bloodadvances.2026020355. [Epub ahead of print]
      Newer approaches to control alloreactivity may produce similar transplant outcomes using HLA-mismatched donors versus HLA-matched unrelated donors. However, prospective comparisons are lacking. BMT CTN 1702 used a donor search prognosis score to assign patients without matched sibling donors, to transplant using an 8/8 HLA-matched unrelated donor (MUD) or the center's preference of haploidentical-related (HAPLO), mismatched unrelated (MMUD), or umbilical cord blood (UCB) donors. Outcomes using MUD were compared to HAPLO, MMUD and UCB while adjusting for relevant covariates. Patients (n=1179) (93% adults) underwent transplantation with a MUD (n=772), HAPLO (n=254), MMUD (n=112) and UCB (n=41) at a median of 3.7, 3.4, 3.9 and 3.8 months from enrollment. Post-transplant cyclophosphamide (PTCy) was used in 23.9%, 83.9%, 65.2% and 0% of MUD, HAPLO, MMUD and UCB HCT. In multivariate analysis, compared to MUD, survival after HCT was significantly lower for patients receiving UCB (HR 2.65, p<0.001) but not statistically different for HAPLO and MMUD HCT recipients (HR 1.08 and 1.18). The risk of relapse was not significantly different by donor type, but treatment-related mortality (TRM) (HR 3.31, p<0.001) and disease-free survival (DFS) (HR 1.99, p=0.002) were inferior for UCB but not different for HAPLO and MMUD than MUD. In PTCy patients, HAPLO and MMUD were associated with increased grade 3/4 acute GVHD (HR 2.39, p=0.017 and 2.53, p=0.038) and chronic GVHD (HR 1.71 each, p=0.028 and 0.080) than MUD, but other outcomes were not different. HAPLO or MMUD may effectively be used to expedite transplantation when finding MUD is unlikely. NCT03904134.
    DOI:  https://doi.org/10.1182/bloodadvances.2026020355
  20. EJHaem. 2026 Jun;7(3): e70301
       Background: Janus kinase inhibitors (JAKis), the current standard of care for myelofibrosis (MF), provide clinical benefit, but responses are frequently incomplete, non-durable, and associated with cytopenias, underscoring the need for therapies with novel mechanisms of action. Selinexor, an oral selective inhibitor of Exportin 1 (XPO1), modulates nuclear-cytoplasmic transport, inflammatory signaling, and cancer cell proliferation.
    Methods: XPORT-MF-035, a global, Phase 2, randomized, open-label study comparing selinexor monotherapy with physician's choice (PC) in MF previously treated with JAKi, randomized patients 1:1 to selinexor or PC, with crossover permitted upon disease progression or inadequate spleen response. Primary endpoint was spleen volume reduction ≥ 35% (SVR35). Additional endpoints included symptom improvement, hematologic outcomes, plasma cytokine analyses, and safety.
    Results: Twenty-four patients were enrolled and treated. In the efficacy-evaluable population, SVR35 at any time was achieved by 29% (2/7) and 13% (1/8) of selinexor- and PC-treated patients, respectively; 8% (1/12) in each arm achieved SVR35 at Week 24 in the intent-to-treat population. Among evaluable patients, 40% (2/5) achieved SVR35 following selinexor crossover. Symptom improvement was observed with selinexor but not PC. Selinexor-treated patients experienced fewer Grade ≥ 3 anemia events with lower transfusion burden and reductions in multiple proinflammatory cytokines. Selinexor was generally well tolerated; common treatment-emergent adverse events (TEAEs) included anemia, asthenia, and decreased weight. One TEAE leading to death occurred in the selinexor and two in PC; none were considered treatment-related.
    Conclusions: Despite limited sample size, XPORT-MF-035 provides descriptive data on the safety, tolerability, and biological activity of selinexor monotherapy in previously treated MF, supporting further evaluation in this population.
    Trial Registration: ClinicalTrials.gov identifier: NCT04562870.
    Keywords:  JAKi; Phase 2; myelofibrosis; randomized; selinexor
    DOI:  https://doi.org/10.1002/jha2.70301