ArticleMolecular therapy. Nucleic acids2024
STAT6-targeting antisense oligonucleotides against solitary fibrous tumor.
Article in Molecular therapy. Nucleic acids, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Construction and Characterization of Paired Patient-Derived Cell Models for Solitary Fibrous Tumors (SFTs).Cancers · 2026Article
- Identification of BET inhibitors (BETi) against solitary fibrous tumor (SFT) through high-throughput screening (HTS).Neoplasia (New York, N.Y.) · 2025Article
- Gene Fusions as Potential Therapeutic Targets in Soft Tissue Sarcomas.Biomolecules · 2025Review
- Lipid Nanovesicles in Cancer Treatment: Improving Targeting and Stability of Antisense Oligonucleotides.Drug design, development and therapy · 2025Review
- Solitary fibrous tumor of the prostate with accompanying low-grade prostate cancer.Urology case reports · 2024Article
- Effective inhibition of dengue virus replication using 3'UTR-targeted Vivo-Morpholinos.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Solitary fibrous tumor (SFT) is a rare, non-hereditary soft tissue sarcoma thought to originate from fibroblastic mesenchymal stem cells. The etiology of SFT is thought to be due to an environmental intrachromosomal gene fusion between NGFI-A-binding protein 2 (NAB2) and signal transducer and activator protein 6 (STAT6) genes on chromosome 12, wherein the activation domain of STAT6 is fused with the DNA-binding domain of NAB2 resulting in the oncogenesis of SFT. All NAB2-STAT6 fusion variations discovered in SFTs contain the C-terminal of STAT6 transcript, and thus can serve as target site for antisense oligonucleotides (ASOs)-based therapies. Indeed, our
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Registered trials
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