ArticleBlood2022
Effective therapy for AML with RUNX1 mutation by cotreatment with inhibitors of protein translation and BCL2.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Efficacy and safety of venetoclax plus azacitidine based regimens in the treatment of relapsed or refractory acute myeloid leukemia: a systematic review and meta-analysis.Annals of hematology · 2025Pooled it
- Wired to Survive: How AML Cytogenetics Shape Apoptotic Dependence and Venetoclax Resistance.Genes · 2026Review
- Multi-omics analysis of pediatric minimally differentiated acute myeloid leukemia reveals RUNX1-driven stemness and chemoresistance.Leukemia · 2026Article
- [Clinical characteristics and prognosis of acute myeloid leukemia patients with RUNX1 single-site and multiple-site gene mutations].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Activation of c-Myc confers resistance to venetoclax via inhibition of Bim in t(8;21)-positive acute myeloid leukemia.Cell communication and signaling : CCS · 2026Article
- Impact of RUNX1 mutations at distinct sites on the clinical characteristics and prognosis of patients with acute myeloid leukemia.BMC cancer · 2026Article
- Histone modification clocks for robust cross-species biological age prediction and elucidating senescence regulation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- [Clinical characteristics of RUNX1-mutated acute myeloid leukemia patients].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- CD71-Targeted and ROS-Responsive Micelles for Homoharringtonine Delivery to Enhance Therapeutic Efficiency Against FLT3-ITD Acute Myeloid Leukemia.International journal of nanomedicine · 2026Article
- Targeted protein degradation: species, diseases and efficient utilization.Journal of translational medicine · 2025Review
- The Dual Role of RUNX1 in Inflammation-Driven Age-Related Diseases: From Molecular Mechanisms to Clinical Translation.Biomedicines · 2025Review
- Article
- Solute carrier-correlated gene signature in predicting the prognosis and immunity in patients with acute myeloid leukemia.European journal of medical research · 2025Article
- Omacetaxine and venetoclax in relapsed/refractory acute myeloid leukemia or myelodysplastic syndrome with mutant RUNX1.Blood neoplasia · 2025Article
- The multiplex crosstalk between non-coding RNAs, programmed cell death and related mechanisms: a dynamic duo in hematological malignancies.Cancer cell international · 2025Review
- Chidamide and cytarabine synergistically treat acute myeloid leukemia: inhibiting ribosome biogenesis via the MYC-RRP9 pathway.Cell death & disease · 2025Article
- Prognostic Risk Model of Megakaryocyte-Erythroid Progenitor (MEP) Signature Based on AHSP and MYB in Acute Myeloid Leukemia.Biomedicines · 2025Article
- Identification of cell adhesion related signature for molecular subtyping and prognostic prediction in acute myeloid leukemia.Discover oncology · 2025Article
- Review
- The epigenetic revolution in hematology: from benchside breakthroughs to clinical transformations.Clinical and experimental medicine · 2025Review
Corrections and comments
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
The majority of RUNX1 mutations in acute myeloid leukemia (AML) are missense or deletion-truncation and behave as loss-of-function mutations. Following standard therapy, AML patients expressing mtRUNX1 exhibit inferior clinical outcome than those without mutant RUNX1. Studies presented here demonstrate that as compared with AML cells lacking mtRUNX1, their isogenic counterparts harboring mtRUNX1 display impaired ribosomal biogenesis and differentiation, as well as exhibit reduced levels of wild-type RUNX1, PU.1, and c-Myc. Compared with AML cells with only wild-type RUNX1, AML cells expressing mtRUNX1 were also more sensitive to the protein translation inhibitor homoharringtonine (omacetaxine) and BCL2 inhibitor venetoclax. Homoharringtonine treatment repressed enhancers and their BRD4 occupancy and was associated with reduced levels of c-Myc, c-Myb, MCL1, and Bcl-xL. Consistent with this, cotreatment with omacetaxine and venetoclax or BET inhibitor induced synergistic in vitro lethality in AML expressing mtRUNX1. Compared with each agent alone, cotreatment with omacetaxine and venetoclax or BET inhibitor also displayed improved in vivo anti-AML efficacy, associated with improved survival of immune-depleted mice engrafted with AML cells harboring mtRUNX1. These findings highlight superior efficacy of omacetaxine-based combination therapies for AML harboring mtRUNX1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.