bims-tremyl Biomed News
on Therapy resistance biology in myeloid leukemia
Issue of 2025–08–24
twenty papers selected by
Paolo Gallipoli, Barts Cancer Institute, Queen Mary University of London



  1. Haematologica. 2025 Jul 31.
      Conflicting data exist on the impact of mismatched unrelated donor (MMUD) compared to matched unrelated donor (MUD) in hematopoietic cell transplantation (HCT) with post-transplant cyclophosphamide (PTCy), highlighting the need for disease-specific research. We conducted a retrospective analysis of donor characteristics in 350 patients with acute lymphoblastic leukemia (ALL) in complete remission (CR) who received 8/8 human leukocyte antigen (HLA)-matched MUD and 7/8 HLA-matched MMUD. The primary endpoint was leukemia-free survival (LFS). The median age was 37 years (range, 18-76), with 231 (66%) in first CR, and 280 (80%) diagnosed with B-cell ALL. The median donor age was 28 years (range, 18-57), with 237 (68%) MUD and 113 (32%) MMUD. The use of MUD or MMUD did not have a significant impact on LFS or other transplant outcomes. Among other donorrelated variables, CMV-negative donor for a CMV-negative recipient was associated with improved LFS (HR 0.55; 95% CI 0.32-0.96) and overall survival (HR 0.52; 95% CI 0.28-1), while older donor age showed an increased risk of acute graft-versus-host disease (GVHD) grade III-IV (HR 1.7; 95% CI 1.1-2.64) and female donor to male recipient combination increased the risk of grade II-IV acute GvHD (HR 1.78; 95% CI 1.05-3). In conclusion, non-HLA donor characteristics rather than HLA matching should be prioritized to guide unrelated donor selection for ALL patients in the PTCy HCT setting.
    DOI:  https://doi.org/10.3324/haematol.2025.287750
  2. Blood Cancer J. 2025 Aug 16. 15(1): 139
      Management paradigms for newly-diagnosed acute myeloid leukemia (ND-AML) in patients considered unfit to receive intensive chemotherapy have evolved with improved understanding of disease biology. In this setting, management requires clear delineation of goals of therapy that should include preservation of quality-of-life (QoL). Combination of venetoclax (Ven) and a hypomethylating agent (HMA) is the current standard-of-care in most circumstances with flexible options in regard to drug dose and duration of treatment as well as the addition (triplet combinations) or alternative use of targeted therapies, such as inhibitors of FLT3, IDH1, IDH2, or menin for patients with NPM1MUT or KMT2A rearrangements (KMT2Ar). Response rates (CR/CRi:40-90%) and overall survival outcomes (3-year: 0-67%) following Ven-HMA therapy are highly variable and depend primarily on tumor genetics while achievement of complete response with (CR) or without count recovery (CRi) and consolidation with allogeneic stem cell transplant (ASCT) are essential in securing long-term survival. Favorable genomic predictors of response to Ven-HMA include NPM1MUT, IDH2MUT, and DDX41MUT, and unfavorable TP53MUT, FLT3-ITD, and K/NRASMUT. Favorable predictors of overall survival include IDH2MUT, and unfavorable TP53MUT, FLT3-ITD, K/NRASMUT, and KMT2Ar. Whether or not triplet regimens provide significant survival gain over Ven-HMA in genetically targetable subgroups remains to be determined. Particularly frail patients who are considered unfit for Ven-HMA might benefit from monotherapy targeting FLT3MUT, IDH1/2MUT, NPM1MUTor KMT2Ar. Future research projects should focus on incorporating patient-reported outcomes in clinical trials, optimization of Ven-HMA dosing and treatment duration especially in triplet combinations and broadening the use of ASCT and clarification of its timing.
    DOI:  https://doi.org/10.1038/s41408-025-01346-1
  3. Bone Marrow Transplant. 2025 Aug 19.
      Allogeneic hematopoietic cell transplantation (alloHCT) from 8/10 HLA-matched unrelated donor is performed in a minority of patients. There is little data on its outcomes and consequently, guidelines on optimal transplantation procedures are lacking. The Transplant complications working party of the EBMT performed a registry study comparing approaches to graft-versus-host disease (GVHD) prophylaxis in recipients of alloHCT from 8/10 HLA-mismatched unrelated donors (8/10 MMUD). The analysis included 450 adult patients with hematological malignancies receiving a first alloHCT between 2015 and 2021, GVHD prophylaxis strategies included ATG in 318 and PTCy in 132 patients. AlloHCT from 8/10 MMUD resulted in 21.1% non-relapse mortality, 28.5% cumulative incidence of relapse, 55.7% overall survival (OS), 50.4% progression-free-survival and 39.8% GVHD-relapse-free survival (GRFS). PTCy decreased the risk of grade II-IV (HR 0.63, 95%CI 0.40-0.99) and III-IV acute GVHD (HR 0.31, 95%CI 0.13-0.74), improved OS (HR 0.63, 95%CI 0.41-0.95) and GRFS (HR 0.65, 95%CI 0.47-0.91). No other differences between the groups were documented. Transplantation from female donors to male recipients increased the incidence of extensive chronic GVHD (HR 2.39, 95%CI 1.10-5.19) and decreased PFS (HR 1.49, 95%CI 1.01-2.20). AlloHCT from 8/10 HLA-matched unrelated donor is feasible and the use of PTCy in GVHD prophylaxis improves outcomes.
    DOI:  https://doi.org/10.1038/s41409-025-02678-z
  4. Br J Haematol. 2025 Aug 18.
      Normal karyotype acute myeloid leukaemia (NK-AML) in children is a heterogeneous subgroup with scarce data on characteristics and prognosis. We investigated NK-AML in a large paediatric AML cohort from four trials of the Nordic Society for Paediatric Haematology and Oncology-Dutch Belgian Hongkong (NOPHO-DBH) group. Among 1476 AML patients, we identified 316 NK-AML patients (21%). NK-AML was characterized by high frequencies of FLT3 internal tandem duplications (ITD, 33%), mutated NPM1 (28%), WT1 (25%) and CEBPA (21%). Five-year event-free survival (EFS) and overall survival (OS) in NK-AML were 52% (95% confidence interval [CI]: 46-58) and 70% (CI: 65-75) respectively. Restricted to NPM1wt cases only (n = 959), NK-AML was associated with unfavourable outcome (relative risk [RR] of EFS = 0.80, p = 0.014; RR of OS = 0.87, p = 0.022). NK-AML with mutated NPM1 had excellent EFS (79%, CI: 66-88) and OS (97%, CI: 88-99), which was not influenced by concomitant FLT3-ITD. In multivariable analysis, mutated NPM1 in NK-AML was associated with favourable EFS (hazard ratio [HR]: 0.24, CI: 0.13-0.43, p < 0.001) and OS (HR: 0.10, CI: 0.03-0.35, p < 0.001). FLT3-ITD was associated with inferior EFS (HR: 1.56, CI: 1.03-2.35, p = 0.035) and OS (HR: 1.91, CI: 1.11-3.31, p = 0.02). We conclude that prognosis in paediatric NK-AML is independently affected by NPM1 and FLT3-ITD status. Further molecular characterization of NK-AML is needed, especially for NPM1wt NK-AML.
    Keywords:  acute myeloid leukaemia; childhood; cytogenetics of leukaemia; prognostic factors
    DOI:  https://doi.org/10.1111/bjh.70094
  5. Leuk Lymphoma. 2025 Aug 19. 1-6
      Patients with AML remain at risk of death after therapy. Our objective was to characterize patients with AML after three years in remission. 453 patients were documented to be alive and in remission 3 years after diagnosis, median follow-up was 7.2 years in this subgroup. 363 (80%) patients were alive at last follow-up, fifty-two (11%) relapsed, 40 died from relapse. Forty-seven (9%) died in remission. Among remission deaths, mutations in FLT3 (64% v 5%) and NPM1 (45% vs 20%) were common (p < 0.01); causes of death included: other cancers (26%), cardiovascular disease (6%), and graft-versus-host disease (6%). After 3 years in remission, the cumulative incidence of relapse was 8% (95%CI 5-11) and death was 11% (95%CI 8-14). Survival after 3 years in remission was similar to a matched general population cohort (p = 0.7). After 3 years in remission, most common causes of death were relapse, other cancer, or cardiovascular disease.
    Keywords:  AML; cause of death; late relapses
    DOI:  https://doi.org/10.1080/10428194.2025.2547984
  6. Hemasphere. 2025 Aug;9(8): e70179
      Inflammation from the hematopoietic compartment is a critical driver of fibrosis and cytopenias in myeloproliferative neoplasms (MPNs). We previously demonstrated that tasquinimod ameliorates the MPN phenotype, reducing splenomegaly and normalizing fibrosis in a JAK2V617F-driven preclinical model. Using bulk RNA sequencing, we now show that tasquinimod primarily targets the malignant JAK2V617F hematopoietic clone, particularly affecting megakaryocytes and monocytes. Tasquinimod downregulates pro-proliferative pathways, MYC targets, and mTORC signaling, while increasing apoptosis in particularly in JAK2V617F mutant cells. Our data reveal that tasquinimod reverses TGFβ-driven fibrotic reprogramming of megakaryocytes and monocytes. This reversal is crucial for mitigating the pro-fibrotic interactions and signaling in the BM, thereby decreasing the activation of stromal cells. Coculture experiments confirm that direct interaction between JAK2V617F hematopoietic cells and mesenchymal stromal cells upregulates S100A8 in stromal cells, independent of TGFβ alone. In line, genetic ablation of S100A9 in the hematopoietic but not stromal compartment significantly improves the MPN phenotype and normalizes BM fibrosis. Our data highlight the hematopoietic origin of the inflammatory signals driving fibrosis. These insights pave the way for potential therapeutic strategies targeting inflammatory signaling pathways in MPN to mitigate fibrosis and improve patient outcomes.
    DOI:  https://doi.org/10.1002/hem3.70179
  7. Blood Adv. 2025 Aug 19. pii: bloodadvances.2025016898. [Epub ahead of print]
      The alarmins, S100A8 (A8) and S100A9 (A9), are low molecular weight proteins belonging to the S100 protein family. A8 and A9 are secreted into the extracellular space and plasma, where they interact with TLR4 (Toll like receptor 4), RAGE (receptor for advanced glycation end products) and CD33. In present studies, we determined the preclinical efficacy of tasquinimod (TQ) against advanced MPN cell lines and patient-derived (PD) CD34+ blastic phase (BP, >5% blasts in PB) MPN cells. TQ induced loss of viability in cell lines and PD MPN-BP cells, but not in normal CD34+ progenitor cells. In TQ-treated PD MPN-AML cells, RNA-Seq analysis showed negative enrichment of the gene-sets of MYC and E2F targets, IL6-JAK-STAT3 signaling, and of inflammatory response. In phenotypically defined, PD, CD34+ MPN-BP stem progenitor cells, CyTOF analysis showed that TQ reduced expression of proteins including A8, A9, and MPO, while increasing expression of GFI1, p21 and cleaved PARP. Co-treatment with TQ and ruxolitinib or BET inhibitor induced synergistic lethality in advanced MPN-BP cells. Monotherapy with TQ significantly improved survival of immune-depleted NSG mice engrafted with PDX cells of MPN-AML. Notably, cotreatment with TQ and ruxolitinib or OTX015 induced significantly greater survival than treatment with single agents in the NSG mice engrafted with the PDX cells. These findings clearly demonstrate the preclinical efficacy of TQ in advanced MPN-BP cells and create the rationale to further interrogate the efficacy of TQ-based combinations with the current, front-line therapies or novel agents in advanced MPNs with excess blasts.
    DOI:  https://doi.org/10.1182/bloodadvances.2025016898
  8. J Clin Oncol. 2025 Aug 18. JCO2500535
    SAL, AMCL-CG, AML-SG, OSHO, PETHEMA, HOVON and GIMEMA study groups
       PURPOSE: The phase III APOLLO trial prospectively compared the efficacy of arsenic trioxide (ATO) in combination with all-trans retinoic acid (ATRA) regimen (ATRA and ATO [ATRA-ATO]) plus low-dose idarubicin versus standard ATRA plus anthracycline-based chemotherapy (ATRA-CHT) regimen (ie, ATRA and idarubicin regimen) in patients with high-risk acute promyelocytic leukemia (APL; EudraCT 2015-01151-68; ClinicalTrials.gov identifier: NCT02688140).
    METHODS: Adult patients with newly diagnosed high-risk APL in the ATRA-ATO arm received ATO 0.15 mg/kg once daily and ATRA 45 mg/m2 twice daily until complete remission (CR), with two doses of idarubicin 12 mg/m2 on days 1 and 3, followed by consolidation therapy (four ATRA-ATO cycles). Patients in the ATRA-CHT arm received induction with ATRA 45 mg/m2 twice daily and idarubicin 12 mg/m2 once daily on days 1, 3, 5, and 7, followed by three cycles of chemotherapy-based consolidation and 2 years of maintenance therapy. The primary study end point was event-free survival (EFS) at 2 years.
    RESULTS: As of July 2022, 133 eligible patients had received either ATRA-ATO (n = 68) or ATRA-CHT (n = 65). The study was discontinued prematurely because of slow accrual during the COVID-19 pandemic. After a median follow-up of 37 months (range, 1.7-88.6 months), 2-year EFS was 88% in the ATRA-ATO arm and 71% in the ATRA-CHT arm (HR, 0.4 [95% CI, 0.17 to 0.92]; log-rank test P = .02). At a median of 7.8 and 12.1 months from achievement of CR, molecular relapse occurred in one (1.5%) ATRA-ATO patient versus eight (12.3%) ATRA-CHT patients (P = .014). Overall, 32% and 68% of patients receiving ATRA-ATO and ATRA-CHT, respectively, reported serious treatment-emergent adverse events (P < .01).
    CONCLUSION: The results of the APOLLO trial support the use of ATO and ATRA for the treatment of newly diagnosed patients with high-risk APL.
    DOI:  https://doi.org/10.1200/JCO-25-00535
  9. Cell Death Differ. 2025 Aug 19.
      Bone marrow failure is a severe complication of human telomere biology disorders and predisposes individuals to secondary leukemia. A deeper understanding of this process could offer significant clinical benefits. Using a preclinical mouse model deficient in the RNA component of the telomerase (mTerc), we demonstrate that bone marrow failure results from excessive apoptosis, predominantly mediated by the pro-apoptotic p53 target PUMA. Genetic ablation of Puma alleviates hematological phenotypes and reduces the risk of lethal bone marrow failure while preserving genomic stability. Mechanistically, PUMA deficiency decreases the sensitivity of hematopoietic cells to lethal stressors, including critically short telomeres. As a consequence, reduced compensatory turnover of hematopoietic progenitors slows down telomere shortening at the population level, delays stem cell exhaustion, and diminishes the acquisition of somatic mutations - ultimately preventing neoplastic transformation. Elevated expression of both p53 and PUMA is also observed in the bone marrow from patients with telomere biology disorders. While apoptosis resistance is traditionally associated with malignant transformation, our findings provide evidence that selective inhibition of PUMA-mediated apoptosis may represent a viable therapeutic strategy to prevent or delay leukemic transformation in this patient population.
    DOI:  https://doi.org/10.1038/s41418-025-01557-w
  10. Br J Pharmacol. 2025 Aug 20.
       BACKGROUND AND PURPOSE: Activation of Protein Phosphatase 2A (PP2A), via genetic and pharmacologic modulation of SET, has recently being identified as a promising strategy to therapeutically target acute myeloid leukaemia (AML) carrying KMT2A (MLL) chromosomal translocations (KMT2A-r AML).
    EXPERIMENTAL APPROACH: In this study, we investigated the expression of PP2A subunits and the therapeutic potential of forskolin, a cyclic adenosine monophosphate (cAMP) elevating natural compound that has been reported as a PP2A activator.
    KEY RESULTS: Our data show that PPP2CA encoding protein phosphatase 2 catalytic subunit α is abundantly expressed in KMT2A-r AML cells. Treatment with forskolin arrests proliferation; induces cell death; represses the expression of MYC, HOXA9 and HOXA10; stimulates PP2A activity; and attenuates the activity of ERK1/2 in KMT2A-r AML cells. Forskolin increases sensitivity to standard-of-care daunorubicin in KMT2A-AML cell lines and PDX. Silencing PPP2CA partially rescues the cytotoxic effect of forskolin, stimulates ERK1/2, inhibits GSK3β, and abolishes the forskolin-mediated repression of c-MYC and HOXA10, but it did not affect the potentiation of response to daunorubicin. This effect was also not dependent on increase of cAMP, but it was because of increase in the intracellular accumulation of daunorubicin, through inhibition of drug efflux pump P-glycoprotein 1 (multidrug resistance protein).
    CONCLUSIONS AND IMPLICATIONS: In conclusion, our findings highlight a novel mechanism of action for forskolin and support a potential role of this natural compound in combination with current conventional agent daunorubicin in the treatment of KMT2A-r AML.
    Keywords:  AML; ERK1/2; GSK3β; HOXA; KMT2A; MDR; MLL; MYC; PP2A; P‐glycoprotein; daunorubicin; forskolin; leukaemia; natural compounds; phosphatase
    DOI:  https://doi.org/10.1111/bph.70158
  11. Blood Adv. 2025 Aug 19. pii: bloodadvances.2025017011. [Epub ahead of print]
      Early clinical experience with the use of chimeric antigen receptor (CAR)-T cell therapies for patients with acute myeloid leukemia (AML) has been beset by high rates of toxicities and low rates of response. We convened an international workshop with the goal of bringing investigators in the field of AML-directed CAR-T cell therapy together to facilitate discussion of roadblocks and to brainstorm potential solutions. Based on discussions at the workshop, it was evident (i) that treating and targeting AML with CAR-T cells is associated with unique clinical challenges, and (ii) that variability in clinical trial design, definitions of toxicities, correlative data collection, and reporting methods hinders the field's ability to compare study outcomes and to develop best practices. Further, details of fundamental CAR-T cell attributes and key correlates of efficacy and toxicity were not uniformly reported in published studies, limiting understanding of barriers to success. These observations led to a concerted team effort in which experts in basic/translational science and clinical investigation from pediatric and adult centers worked together to streamline key attributes of clinical trial design and reporting. Consensus criteria were discussed and agreed upon leading to the creation of a white paper. These guidelines aim to bolster the overall quality of AML-directed CAR-T cell research, allow for comparisons across trials and to inform the next phase of development of AML-directed CAR-T cell therapies that we hope will improve patient outcomes.
    DOI:  https://doi.org/10.1182/bloodadvances.2025017011
  12. Genome Biol. 2025 Aug 19. 26(1): 253
       BACKGROUND: KAT6A-CBP (K/C) and KAT6A-P300 (K/P) fusions are recurrent genetic alterations in acute myeloid leukemia (AML) associated with poor prognosis. Despite their strong oncogenic potential, the mechanisms underlying their genomic targeting and leukemogenic function remain unclear. A major challenge has been their large size, which has impeded preclinical model development and mechanistic studies.
    RESULTS: We employ a domain-focused truncation strategy to generate de novo murine models of K/C and K/P fusions, which faithfully recapitulate the morphological, immunophenotypic, and transcriptomic features of KAT6A-rearranged AML. Genomic profiling reveals that KAT6A fusions preferentially localize to H3K4me2/3-marked regions, while biochemical analyses uncover that KAT6A interacts with the Nucleosome Remodeling Factor (NURF), a key H3K4me2/3 reader. Disrupting NURF-chromatin interactions via depletion or small-molecule inhibition of its subunit, Bromodomain PHD Finger Transcription Factor (BPTF), impairs K/C recruitment and disrupts MLL/COMPASS-mediated H3K4me2 deposition, defining a functional epigenetic module involving KAT6A chimeras, NURF, and MLL/COMPASS. Notably, CBP/P300 inhibition reduces histone acetylation and chromatin accessibility, further impairing the recruitment of this epigenetic module. Targeting this module via NURF or CBP/P300 inhibition demonstrates efficacy in K/C leukemia models, with enhanced therapeutic effects observed when combined.
    CONCLUSIONS: Our study identifies a self-reinforcing epigenetic module of histone modifiers and readers in KAT6A-rearranged AML, providing mechanistic insights into the genomic targeting of KAT6A chimeras and highlighting promising combinatorial therapeutic strategies.
    Keywords:  AML; Acute myeloid leukemia; Chromatin accessibility; KAT6A; KAT6A-CBP; KAT6A-P300; MLL/COMPASS; NURF; Nucleosome Remodeling Factor
    DOI:  https://doi.org/10.1186/s13059-025-03743-y
  13. Blood. 2025 Aug 19. pii: blood.2024027692. [Epub ahead of print]
      Acute myeloid leukemia (AML) is a highly heterogeneous hematological malignancy that increasingly affects the elderly population, with its post-transcriptional landscape remaining largely elusive. Establishing a stable proteomics-based classification system and systematically screening age-related proteins and regulatory networks are crucial for understanding the pathogenesis and outcomes of AML. In this study, we leveraged a multi-omics cohort of 374 newly diagnosed AML patients, integrating proteome, phosphoproteome, genome, transcriptome, and drug screening data. Through similarity network fusion clustering, we established eight proteomic subtypes with distinct clinical and molecular properties, including S1 (CEBPA mutations), S3 (myelodysplasia-related AML), S4 (PML::RARA), S5 (NPM1 mutations), S6 (PML::RARA and RUNX1::RUNX1T1), S8 (CBFB::MYH11), S2 and S7 (mixed), aligning well with and adding actionable value to the latest World Health Organization nomenclature of AML. Hematopoietic lineage profiling of proteins indicated that megakaryocyte/platelet- and immune-related networks characterized distinct aging patterns in AML, which were consistent with our recent findings at the RNA level. Phosphosites also demonstrated distinct age-related features. The high protein abundance of megakaryocytic signatures was observed in S2, S3, and S7 subtypes, which were associated with advanced age and dismal prognosis of patients. A hematopoietic aging score with an independent prognostic value was established based on proteomic data, where higher scores correlated with myelodysplasia-related AML, NPM1 mutations, and clonal hematopoiesis-related gene mutations. Collectively, this study provides an overview of the molecular circuits and regulatory networks of AML during the aging process, advancing current classification systems and offering a comprehensive perspective on the disease.
    DOI:  https://doi.org/10.1182/blood.2024027692
  14. Blood Neoplasia. 2025 Aug;2(3): 100137
      Mutations in the histone methyltransferase enhancer of zeste homolog 2 (EZH2), particularly the neomorphic Y641F hot spot mutation, are implicated in hematologic malignancies. However, how developmental timing and cellular context influence their oncogenic potential remains poorly understood. Here, we used a conditional Ezh2 Y641F allele with multiple tissue-specific Cre drivers to investigate the effects of these mutations across hematopoietic development. We found that ubiquitous or early expression of Ezh2 Y641F led to bone marrow failure and reduced survival with no evidence of transformation. In contrast, expression in committed B cells using CD19-Cre consistently induced B-cell lymphomas, underscoring a context- and stage-specific requirement for transformation. Transcriptomic analysis of B-cell progenitors revealed distinct gene expression changes between Cre models, including interferon signaling and upregulation of guanylate-binding proteins (GBPs) in Mx1-Cre Ezh2 Y641F mutants. We identified a redistribution of histone 3 lysine 27 trimethylation at the GBP locus and showed that GBP2 overexpression impairs multilineage hematopoiesis by promoting apoptosis and skewing differentiation. These findings demonstrate that the oncogenic potential of Ezh2 Y641F is highly dependent on the cellular environment in which it is expressed and that the timing of mutation acquisition critically shapes the impact of EZH2 on hematopoiesis and disease outcome.
    DOI:  https://doi.org/10.1016/j.bneo.2025.100137
  15. Biomaterials. 2025 Aug 08. pii: S0142-9612(25)00531-9. [Epub ahead of print]325 123612
      Hematopoietic stem cell (HSC) transplantation to treat haematological disorders is greatly restricted by poor cell availability. Engineering of culture platforms that mimic the physiological properties of the bone marrow (BM) in a scalable format is important to enable the translation of HSC therapies. Here, we report the design of biomimetic BM niches enabling the culture of HSCs in a scalable 3D platform. Beyond cellular and biochemical components (e.g. matrix and growth factors), an important element of the BM microenvironment is its architecture, dense in adipocytes, with relatively limited matrix and anisotropic mechanical properties. To capture this context, we propose the use of bioemulsions1,2 in which oil microdroplets and associated mechanical anisotropy recreate important architectural features of the hematopoietic niche. Mesenchymal stem cells (MSCs) grown at the surface of bioemulsions assembled an interstitial matrix and secreted important factors critical to the maintenance of HSC phenotype. HSCs cultured in the resulting artificial BM niches maintained stemness whilst expanding significantly (>33-fold compared to suspension cultures) and enabling scale up of expansion in conical flask bioreactors (2 M cell batches). This platform harnesses engineered BM microenvironments and the processability of microdroplet technologies to produce HSCs in a scalable format, for application in cell-based therapies.
    Keywords:  2D nanomaterials; Liquid-liquid interface; Protein nanosheet; Self-assembly; Stem cells; Toughness
    DOI:  https://doi.org/10.1016/j.biomaterials.2025.123612
  16. Cell Death Differ. 2025 Aug 16.
      The N6-methyladenosine (m6A) modification plays an important role in the pathogenesis of various myeloid malignancies. However, its specific role in RAS mutation-induced myeloid malignancy is incompletely understood. In this study, we found that m6A methyltransferase methyltransferase-like 14 (METTL14) was highly expressed and associated with a shorter survival in a RAS-mutation myeloid malignancy, juvenile myelomonocytic leukemia (JMML). The knockout of METTL14 was revealed to significantly promote hematopoietic stem/progenitor cells (HSPCs) expansion and suppresses disease progression in a KrasG12D/+ mutation-induced mouse model of JMML. Moreover, knockout of METTL14 reduces hyperproliferation of KrasG12D/+ HSPCs and suppresses oncogenic KrasG12D/+-induced myeloid disease in a cell-autonomous manner. Mechanistically, we revealed that the knockout of METTL14 reduced the autophagy levels of HSPCs by suppressing the transcription and translation of autophagy-related genes, such as autophagy-related gene 5 (Atg5) and autophagy-related gene 9 (Atg9a), through m6A modification. Furthermore, we found that the autophagy inhibition through knockout of ATG5 in KrasG12D/+ mutant mice promoted the expansion of HSPCs and inhibited the progression of leukemia disease, consistent with the phenotypes of knockout of METTL14. Finally, we observed that combined treatment with a m6A inhibitor and a MEK inhibitor synergistically suppressed JMML growth. Collectively, these findings highlight the critical role of METTL14 in JMML tumorigenesis and suggest that m6A modification represents a promising therapeutic target for this disease.
    DOI:  https://doi.org/10.1038/s41418-025-01561-0
  17. Lancet Reg Health West Pac. 2025 Aug;61 101664
       Background: Outcomes of older patients with acute myeloid leukemia (AML) undergoing allogeneic hematopoietic stem-cell transplantation (allo-HSCT) remain unsatisfactory. The primary objective of this trial was to establish whether decitabine combined with reduced-intensity conditioning (RIC) regimen could improve overall survival (OS) for this population in composite complete remission (CRc).
    Methods: We conducted a single-arm, phase 2 trial at six hospitals in China. Eligible patients were aged 60-80 years, had a diagnosis of AML, achieved CRc at transplantation, were willing to undergo the first allo-HSCT, and had an Eastern Cooperative Oncology Group performance status of 0-2. Patients received decitabine combined with RIC regimen, comprising decitabine 20 mg/m2 daily intravenously (days -9 to -7), busulfan 3.2 mg/kg daily intravenously (days -5 to -4), and fludarabine 30 mg/m2 daily intravenously (days -6 to -3). The primary endpoint was 2-year OS rate. All efficacy and safety endpoints were assessed in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT03530085) and is complete.
    Findings: Between Jan 1, 2021 and Nov 30, 2022, 60 patients were enrolled. With a median follow-up of 35.5 months (IQR 32.5-39.2), 39 patients survived and 21 died. The 2-year OS rate was 67% (95% CI 56-80), which met the primary objective. Within 100 days post-transplantation, the most common grade 3-4 non-hematological treatment-emergent adverse events (TEAEs) were infections (22 [37%]), acute graft-versus-host disease (21 [35%]), and gastrointestinal disorders (16 [27%]). Five (8%) patients died of TEAEs, with one death treatment-related.
    Interpretation: Decitabine combined with RIC regimen exhibits encouraging OS and acceptable toxicity profile, which might be a suitable therapeutic option for older patients with AML.
    Funding: National Natural Science Foundation of China; Science and Technology Program of Guangdong Province; National Key Research and Development Program of China.
    Keywords:  Acute myeloid leukemia; Allogeneic hematopoietic stem cell transplantation; Decitabine; Older; Reduced-intensity conditioning
    DOI:  https://doi.org/10.1016/j.lanwpc.2025.101664
  18. Cell. 2025 Aug 14. pii: S0092-8674(25)00856-6. [Epub ahead of print]
      RNA Pol II-mediated transcription is essential for eukaryotic life. Although loss of transcription is thought to be universally lethal, the associated mechanisms promoting cell death are not yet known. Here, we show that death following the loss of RNA Pol II activity does not result from dysregulated gene expression. Instead, it occurs in response to loss of the hypophosphorylated form of Rbp1 (also called RNA Pol IIA). Loss of RNA Pol IIA exclusively activates apoptosis, and expression of a transcriptionally inactive version of Rpb1 rescues cell viability. Using functional genomics, we identify the mechanisms driving lethality following the loss of RNA Pol IIA, which we call the Pol II degradation-dependent apoptotic response (PDAR). Using the genetic dependencies of PDAR, we identify clinically used drugs that owe their lethality to a PDAR-dependent mechanism. Our findings unveil an apoptotic signaling response that contributes to the efficacy of a wide array of anti-cancer therapies.
    Keywords:  BCL2L12; DNA damage; PTBP1; RNA polymerase II; apoptosis; cancer therapy; cell death; chemotherapy; cisplatin; transcription
    DOI:  https://doi.org/10.1016/j.cell.2025.07.034