ArticleJournal of leukocyte biology2021
MDS-associated SF3B1 mutations enhance proinflammatory gene expression in patient blast cells.
Article in Journal of leukocyte biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Using cell-specific late-phase asthma mRNA biomarkers to repurpose drugs that concurrently reverse disease signatures across multiple immune cell-types.PLoS computational biology · 2026Article
- Inflammatory stromal and T cells mediate human bone marrow niche remodeling in clonal hematopoiesis and myelodysplasia.Nature communications · 2025Article
- Meeting Report From the 2024 Symposium on IRAK4 in Cancer: Highlights and Clinical Updates.Clinical lymphoma, myeloma & leukemia · 2025Review
- A Case of High-Risk Myelodysplastic Syndrome With Cryoglobulinemia, Hemophagocytic Lymphohistiocytosis, and Progression to Multiple Organ Failure.Journal of medical cases · 2025Article
- Low-risk MDS-A spotlight on precision medicine forHemaSphere · 2025Review
- Implications for metabolic disturbances in myelodysplastic syndromes.Seminars in hematology · 2024Review
- Article
- The immunoregulatory role of monocytes and thrombomodulin in myelodysplastic neoplasms.Frontiers in oncology · 2024Review
- SF3B1 mutations in myelodysplastic syndromes: A potential therapeutic target for modulating the entire disease process.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Two factors known to contribute to the development of myelodysplastic syndrome (MDS) and other blood cancers are (i) somatically acquired mutations in components of the spliceosome and (ii) increased inflammation. Spliceosome genes, including SF3B1, are mutated at high frequency in MDS and other blood cancers; these mutations are thought to be neomorphic or gain-of-function mutations that drive disease pathogenesis. Likewise, increased inflammation is thought to contribute to MDS pathogenesis; inflammatory cytokines are strongly elevated in these patients, with higher levels correlating with worsened patient outcome. In the current study, we used RNAseq to analyze pre-mRNA splicing and gene expression changes present in blast cells isolated from MDS patients with or without SF3B1 mutations. We determined that SF3B1 mutations lead to enhanced proinflammatory gene expression in these cells. Thus, these studies suggest that SF3B1 mutations could contribute to MDS pathogenesis by enhancing the proinflammatory milieu in these patients.
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Registered trials
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