ArticleLeukemia2021
Asxl1 C-terminal mutation perturbs neutrophil differentiation in zebrafish.
Article in Leukemia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- The Disordered Region of ASXL1 Acts as an Auto-Regulator Through Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unleashed condensation by recurrent mutations of an epigenetic regulator promotes cancer.bioRxiv : the preprint server for biology · 2026Article
- Vulnerability of SRSF2-mutated chronic myelomonocytic leukemia to perturbation of the cGAS-STING pathway.Blood advances · 2026Article
- asxl1 C-terminal truncation and SRSF2 mutation drive leukemogenesis via immune reprogramming.Leukemia · 2025Article
- ASXL1 mutation-related clonal hematopoiesis and age-related diseases: clinical evidence and molecular insights.International journal of hematology · 2025Review
- Hotspot gene mutations and treatment response in myelodysplastic syndromes (MDS): predictive biomarkers and targeted strategies.Frontiers in medicine · 2025Review
- How CBX proteins regulate normal and leukemic blood cells.FEBS letters · 2024Review
- CXCL8 secreted by immature granulocytes inhibits WT hematopoiesis in chronic myelomonocytic leukemia.The Journal of clinical investigation · 2024Article
- Mutational cooperativity of RUNX1::RUNX1T1 isoform 9a and oncogenic NRAS in zebrafish myeloid leukaemia.Biology open · 2024Article
- Atypical chronic myeloid leukemia found in a patient with eosinophilia for six years: a case report.BMC geriatrics · 2024Article
- Zebrafish Mbd5 binds to RNA m5C and regulates histone deubiquitylation and gene expression in development metabolism and behavior.Nucleic acids research · 2024Article
- Multiomics of Bohring-Opitz syndrome truncating ASXL1 mutations identify canonical and noncanonical Wnt signaling dysregulation.JCI insight · 2023Article
- Transgenic IDH2Oncogene · 2023Article
- The Contribution of the Zebrafish Model to the Understanding of Polycomb Repression in Vertebrates.International journal of molecular sciences · 2023Review
- Learning from Zebrafish Hematopoiesis.Advances in experimental medicine and biology · 2023Review
- ASXL1/2 mutations and myeloid malignancies.Journal of hematology & oncology · 2022Review
- Molecular Classification and Overcoming Therapy Resistance for Acute Myeloid Leukemia with Adverse Genetic Factors.International journal of molecular sciences · 2022Review
- Whole-genome sequencing illuminates multifaceted targets of selection to humic substances in Eurasian perch.Molecular ecology · 2022Article
- Zebrafish models of inflammation in hematopoietic development and disease.Frontiers in cell and developmental biology · 2022Review
- The Functions and Mechanisms of PR-DUB in Malignancy.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ASXL1 is one of the most frequently mutated genes in malignant myeloid diseases. In patients with myeloid malignancies, ASXL1 mutations are usually heterozygous frameshift or nonsense mutations leading to C-terminal truncation. Current disease models have predominantly total loss of ASXL1 or overexpressed C-terminal truncations. These models cannot fully recapitulate leukemogenesis and disease progression. We generated an endogenous C-terminal-truncated Asxl1 mutant in zebrafish that mimics human myeloid malignancies. At the embryonic stage, neutrophil differentiation was explicitly blocked. At 6 months, mutants initially exhibited a myelodysplastic syndrome-like phenotype with neutrophilic dysplasia. At 1 year, about 13% of mutants further acquired the phenotype of monocytosis, which mimics chronic myelomonocytic leukemia, or increased progenitors, which mimics acute myeloid leukemia. These features are comparable to myeloid malignancy progression in humans. Furthermore, transcriptome analysis, inhibitor treatment, and rescue assays indicated that asxl1-induced neutrophilic dysplasia was associated with reduced expression of bmi1a, a subunit of polycomb repressive complex 1 and a reported myeloid leukemia-associated gene. Our model demonstrated that neutrophilic dysplasia caused by asxl1 mutation is a foundation for the progression of myeloid malignancies, and illustrated a possible effect of the Asxl1-Bmi1a axis on regulating neutrophil development.
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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.