ArticleNature communications2017
ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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Who cites it
40 citing papers in PubMed, 68 citations in OpenAlex.
- Fusion gene map of acute leukemia revealed by transcriptome sequencing of a consecutive cohort of 1000 cases in a single center.Blood cancer journal · 2021Trial
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
- Chronic Hypoxia Disrupts Spermatogenesis Through ASXL2-EZH2-Mediated Microtubule Destabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Fusion-specific co-mutational architecture and treatment-response associations in pediatric core-binding factor acute myeloid leukemia: a multicenter exome-profiled cohort.Frontiers in oncology · 2026Article
- Genetic Variants Associated with Suspected Neonatal Hypoxic Ischaemic Encephalopathy: A Study in a South African Context.International journal of molecular sciences · 2025Article
- Single-cell CRISPR screening characterizes transcriptional deregulation in T-cell acute lymphoblastic leukemia.Haematologica · 2024Article
- Additional Sex Combs-like Family Associated with Epigenetic Regulation.International journal of molecular sciences · 2024Review
- B-cell intrinsic regulation of antibody mediated immunity by histone H2A deubiquitinase BAP1.Frontiers in immunology · 2024Article
- Prognosis and risk factors for ASXL1 mutations in patients with newly diagnosed acute myeloid leukemia and myelodysplastic syndrome.Cancer medicine · 2024Article
- Risk-directed therapy based on genetics and MRD improves the outcomes of AML1-ETO-positive AML patients, a multi-center prospective cohort study.Blood cancer journal · 2023Article
- BAP1 promotes osteoclast function by metabolic reprogramming.Nature communications · 2023Article
- A newborn with a pathogenic variant in ASXL2 expanding the phenotype of SHAPNS: a case report and literature review.Translational pediatrics · 2023Article
- Role of ASXL1 in hematopoiesis and myeloid diseases.Experimental hematology · 2022Review
- CARM1-mediated methylation of ASXL2 impairs tumor-suppressive function of MLL3/COMPASS.Science advances · 2022Article
- ASXL1/2 mutations and myeloid malignancies.Journal of hematology & oncology · 2022Review
- The dual role of autophagy in acute myeloid leukemia.Journal of hematology & oncology · 2022Review
- Network inference with Granger causality ensembles on single-cell transcriptomics.Cell reports · 2022Article
- Article
- Review
- KDM4B promotes acute myeloid leukemia associated with AML1-ETO by regulating chromatin accessibility.FASEB bioAdvances · 2021Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Additional sex combs-like (ASXL) proteins are mammalian homologues of additional sex combs (Asx), a regulator of trithorax and polycomb function in Drosophila. While there has been great interest in ASXL1 due to its frequent mutation in leukemia, little is known about its paralog ASXL2, which is frequently mutated in acute myeloid leukemia patients bearing the RUNX1-RUNX1T1 (AML1-ETO) fusion. Here we report that ASXL2 is required for normal haematopoiesis with distinct, non-overlapping effects from ASXL1 and acts as a haploinsufficient tumour suppressor. While Asxl2 was required for normal haematopoietic stem cell self-renewal, Asxl2 loss promoted AML1-ETO leukemogenesis. Moreover, ASXL2 target genes strongly overlapped with those of RUNX1 and AML1-ETO and ASXL2 loss was associated with increased chromatin accessibility at putative enhancers of key leukemogenic loci. These data reveal that Asxl2 is a critical regulator of haematopoiesis and mediates transcriptional effects that promote leukemogenesis driven by AML1-ETO.
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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 OpenQuestion graph.