ReviewGenes & development2016
Spliceosomal gene mutations in myelodysplasia: molecular links to clonal abnormalities of hematopoiesis.
Review in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 110 citations in OpenAlex.
- Safety and activity of selinexor in patients with myelodysplastic syndromes or oligoblastic acute myeloid leukaemia refractory to hypomethylating agents: a single-centre, single-arm, phase 2 trial.The Lancet. Haematology · 2020Trial
- The minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses in Drosophila melanogaster.Nature communications · 2026Article
- Review
- BRD9 depletion-mediated ALOX5 upregulation via chromatin dysregulation induces ferroptosis in SF3B1-mutant hematopoiesis.International journal of hematology · 2026Article
- Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment.The Journal of clinical investigation · 2026Article
- Myelodysplastic Neoplasms (MDS): Pathogenesis and Therapeutic Prospects.Biomolecules · 2025Review
- Identification of UBA7 expression downregulation in myelodysplastic neoplasm with SF3B1 mutations.Scientific reports · 2025Article
- Relevant Developments in the Use of Three-Component Reactions for the Total Synthesis of Natural Products. The last 15 Years.ChemistryOpen · 2024Review
- A mitochondrial surveillance mechanism activated bybioRxiv : the preprint server for biology · 2024Article
- Impaired dNKAP function drives genome instability and tumorigenic growth in Drosophila epithelia.Journal of molecular cell biology · 2024Article
- U2AF1 in various neoplastic diseases and relevant targeted therapies for malignant cancers with complex mutations (Review).Oncology reports · 2024Review
- BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state.Nature communications · 2023Article
- Single-cell multi-omics defines the cell-type-specific impact of splicing aberrations in human hematopoietic clonal outgrowths.Cell stem cell · 2023Article
- Article
- Histidine N1-position-specific methyltransferase CARNMT1 targets C3H zinc finger proteins and modulates RNA metabolism.Genes & development · 2023Article
- Article
- CAR-T: What Is Next?Cancers · 2023Review
- SF3B1 mutations in myelodysplastic syndromes: A potential therapeutic target for modulating the entire disease process.Frontiers in oncology · 2023Review
- Article
- A dual role for the RNA helicase DHX34 in NMD and pre-mRNA splicing and its function in hematopoietic differentiation.RNA (New York, N.Y.) · 2022Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Genomic analyses of the myeloid malignancies and clonal disorders of hematopoiesis that may give rise to these disorders have identified that mutations in genes encoding core spliceosomal proteins and accessory regulatory splicing factors are among the most common targets of somatic mutations. These spliceosomal mutations often occur in a mutually exclusive manner with one another and, in aggregate, account for the most frequent class of mutations in patients with myelodysplastic syndromes (MDSs) in particular. Although substantial progress has been made in understanding the effects of several of these mutations on splicing and splice site recognition, functional connections linking the mechanistic changes in splicing induced by these mutations to the phenotypic consequences of clonal and aberrant hematopoiesis are not yet well defined. This review describes our current understanding of the mechanistic and biological effects of spliceosomal gene mutations in MDSs as well as the regulation of splicing throughout normal hematopoiesis.
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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.