ReviewFrontiers in oncology2023
SF3B1 mutations in myelodysplastic syndromes: A potential therapeutic target for modulating the entire disease process.
Review in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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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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
26 citing papers in PubMed, 27 citations in OpenAlex.
- Splicing-driven post-translational dysregulation: a new frontier for precision cancer medicine and immunotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Inflammatory Signatures in MDS: The Missing Link Between Genetics, Microenvironment, and Therapy.Cells · 2026Review
- Variant-specific SF3B1 mutations drive distinct splicing and mitochondrial dysfunction in myelodysplastic neoplasms.Human genomics · 2026Article
- Role of alternative splicing in cancer progression.Irish journal of medical science · 2026Review
- IGF2BP3 inhibition: another home run for RNA-binding protein targeting in hematological malignancies.Haematologica · 2026Article
- Potential diagnostic, prognostic, and therapeutic implications of ferroptosis in myelodysplastic syndromes.Discover oncology · 2026Review
- Comparative Phosphoproteomic Profiling and Network-based Interactome Analysis of GRK5 and GRK6.Cell biochemistry and biophysics · 2026Article
- A Yeast-Based High-Throughput Screening Platform for the Discovery of Novel pre-mRNA Splicing Modulators.ACS chemical biology · 2026Article
- Genetic landscape of cancer: mechanisms, key genes, and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Emerging trends in bone marrow organoid research: From hematopoietic microenvironment reconstruction to translational and regenerative theranostic applications.Theranostics · 2026Review
- Unlocking the undruggable spliceosome: generative AI and structural dynamics in cancer therapy.Frontiers in cell and developmental biology · 2026Review
- Precursor RNA structural patterns at SF3B1 mutation sensitive cryptic 3' splice sites.RNA biology · 2025Article
- Novel agents and evolving strategies for anemia management in lower-risk myelodysplastic syndromes.Blood research · 2025Review
- Humanized mouse models in MDS.Cell death & disease · 2025Review
- Real-life experience of luspatercept in transfusion-dependent lower risk myelodysplastic syndrome patients.British journal of haematology · 2025Article
- Progress in the Genetics of Myelodysplastic Syndromes with a Latin American Perspective.Genes · 2025Review
- Low-risk MDS-A spotlight on precision medicine forHemaSphere · 2025Review
- Covalent targeting of splicing in T cells.Cell chemical biology · 2025Article
- Molecular Features and Treatment Paradigms of Acute Myeloid Leukemia.Biomedicines · 2024Review
- Treatment of Anemia in Lower-Risk Myelodysplastic Syndrome.Current treatment options in oncology · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelodysplastic syndromes (MDS) are clonal hematologic malignancies characterized by ineffective hematopoiesis and dysplasia of the myeloid cell lineage and are characterized by peripheral blood cytopenia and an increased risk of transformation to acute myeloid leukemia (AML). Approximately half of the patients with MDS have somatic mutations in the spliceosome gene. Splicing Factor 3B Subunit 1A (SF3B1), the most frequently occurring splicing factor mutation in MDS is significantly associated with the MDS-RS subtype. SF3B1 mutations are intimately involved in the MDS regulation of various pathophysiological processes, including impaired erythropoiesis, dysregulated iron metabolism homeostasis, hyperinflammatory features, and R-loop accumulation. In the fifth edition of the World Health Organization (WHO) classification criteria for MDS, MDS with SF3B1 mutations has been classified as an independent subtype, which plays a crucial role in identifying the disease phenotype, promoting tumor development, determining clinical features, and influencing tumor prognosis. Given that SF3B1 has demonstrated therapeutic vulnerability both in early MDS drivers and downstream events, therapy based on spliceosome-associated mutations is considered a novel strategy worth exploring in the future.
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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.