ArticleNature communications2017
Loss of Asxl2 leads to myeloid malignancies in mice.
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 21 papers.
What it found
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
- Review
- Clinical Variability of Shashi-Pena Syndrome: A NovelMolecular syndromology · 2025Article
- Integrative analysis of ASXL family genes reveals ASXL2 as an immunoregulatory molecule in head and neck squamous cell carcinoma.Scientific reports · 2024Article
- Additional Sex Combs-like Family Associated with Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Prognosis and risk factors for ASXL1 mutations in patients with newly diagnosed acute myeloid leukemia and myelodysplastic syndrome.Cancer medicine · 2024Article
- Identification of a de novo variant in the ASXL2 gene related to Shashi-Pena syndrome.Molecular genetics & genomic medicine · 2023Article
- A newborn with a pathogenic variant in ASXL2 expanding the phenotype of SHAPNS: a case report and literature review.Translational pediatrics · 2023Article
- Predicting leukemic transformation in myelodysplastic syndrome using a transcriptomic signature.Frontiers in genetics · 2023Article
- Role of ASXL1 in hematopoiesis and myeloid diseases.Experimental hematology · 2022Review
- ASXL1/2 mutations and myeloid malignancies.Journal of hematology & oncology · 2022Review
- Review
- Understanding the phenotypic spectrum of ASXL-related disease: Ten cases and a review of the literature.American journal of medical genetics. Part A · 2021Article
- HOXBLINC long non-coding RNA activation promotes leukemogenesis in NPM1-mutant acute myeloid leukemia.Nature communications · 2021Article
- Identification of Candidate Biomarker ASXL2 and Its Predictive Value in Pancreatic Carcinoma.Frontiers in oncology · 2021Article
- Myeloid-specific Asxl2 deletion limits diet-induced obesity by regulating energy expenditure.The Journal of clinical investigation · 2020Article
- The role of ASXL1 in hematopoiesis and myeloid malignancies.Cellular and molecular life sciences : CMLS · 2019Review
- Chromatin regulator Asxl1 loss and Nf1 haploinsufficiency cooperate to accelerate myeloid malignancy.The Journal of clinical investigation · 2018Article
- ASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion.Haematologica · 2018Article
- Transcriptome-wide analysis uncovers the targets of the RNA-binding protein MSI2 and effects of MSI2's RNA-binding activity on IL-6 signaling.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 4 institutions in 2 countries.
Funding
Abstract
ASXL2 is frequently mutated in acute myeloid leukaemia patients with t(8;21). However, the roles of ASXL2 in normal haematopoiesis and the pathogenesis of myeloid malignancies remain unknown. Here we show that deletion of Asxl2 in mice leads to the development of myelodysplastic syndrome (MDS)-like disease. Asxl2
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Identifiers
What OpenQuestion holds
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.