ArticleLeukemia2022
Concurrent Zrsr2 mutation and Tet2 loss promote myelodysplastic neoplasm in mice.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Diagnostic Challenges in a Young Man with a Suspected Mast Cell Disorder, Dysplastic Bone Marrow Morphology, and aHematology reports · 2025Article
- ZRSR2 loss causes aberrant splicing in JAK2HemaSphere · 2025Article
- Article
- Humanized mouse models in MDS.Cell death & disease · 2025Review
- Article
- Alternative Splicing: A Potential Therapeutic Target in Hematological Malignancies.Hematology reports · 2024Review
- Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA splicing and epigenetic gene mutations are the most frequent genetic lesions found in patients with myelodysplastic neoplasm (MDS). About 25% of patients present concomitant mutations in such pathways, suggesting a cooperative role in MDS pathogenesis. Importantly, mutations in the splicing factor ZRSR2 frequently associate with alterations in the epigenetic regulator TET2. However, the impact of these concurrent mutations in hematopoiesis and MDS remains unclear. Using CRISPR/Cas9 genetically engineered mice, we demonstrate that Zrsr2
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Registered trials
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