ReviewInternational journal of hematology2017
Splicing factor mutations in MDS RARS and MDS/MPN-RS-T.
Review in International journal of hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting pre-mRNA splicing in cancers: roles, inhibitors, and therapeutic opportunities.Frontiers in oncology · 2023Review
- Review
- Aberrant RNA splicing and therapeutic opportunities in cancers.Cancer science · 2022Review
- Mutations in the RNA Splicing Factor SF3B1 Promote Tumorigenesis through MYC Stabilization.Cancer discovery · 2020Article
- FF-10501 induces caspase-8-mediated apoptotic and endoplasmic reticulum stress-mediated necrotic cell death in hematological malignant cells.International journal of hematology · 2019Article
- The splicing factor Sf3b1 regulates erythroid maturation and proliferation via TGFβ signaling in zebrafish.Blood advances · 2019Article
- Coexistence of Myeloid and Lymphoid Neoplasms: A Single-Center Experience.Advances in hematology · 2019Article
- Impact of splicing factor mutations on clinical features in patients with myelodysplastic syndromes.International journal of hematology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spliceosomal mutations, especially mutations in SF3B1, are frequently (>80%) identified in patients with refractory anemia with ringed sideroblasts (RARS) and myelodysplastic/myeloproliferative neoplasms with ringed sideroblasts and thrombocytosis (MDS/MPN-RS-T; previously known as RARS-T), and SF3B1 mutations have a high positive predictive value for disease phenotype with ringed sideroblasts. These observations suggest that SF3B1 mutations play important roles in the pathogenesis of these disorders and formation of ringed sideroblasts. Here we will review recent insights into the molecular mechanisms of mis-splicing caused by mutant SF3B1 and the pathogenesis of RSs in the context of congenital sideroblastic anemia as well as RARS with SF3B1 mutations. We will also discuss therapy of SF3B1 mutant MDS, including novel approaches.
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