ArticleCancers2023
Reduction of Tumor Growth with RNA-Targeting Treatment of the NAB2-STAT6 Fusion Transcript in Solitary Fibrous Tumor Models.
Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Construction and Characterization of Paired Patient-Derived Cell Models for Solitary Fibrous Tumors (SFTs).Cancers · 2026Article
- RNA-based precision medicine in glioblastoma driven by oncogenic gene fusions.Molecular therapy. Oncology · 2026Review
- Systemic Therapy for Solitary Fibrous Tumor.Current treatment options in oncology · 2026Review
- Pancreatic Solitary Fibrous Tumor: A Common Tumor Occurring in a Rare Location.The American journal of case reports · 2026Article
- Choosing the right animal model for sarcoma research.Cellular and molecular life sciences : CMLS · 2026Review
- Primary orbital solitary fibrous tumor with an 18-year course of five recurrences and extensive sinonasal metastasis following eyeball enucleation: a case report.Frontiers in medicine · 2026Article
- Identification of BET inhibitors (BETi) against solitary fibrous tumor (SFT) through high-throughput screening (HTS).Neoplasia (New York, N.Y.) · 2025Article
- Article
- Advances in the molecular biology of the solitary fibrous tumor and potential impact on clinical applications.Cancer metastasis reviews · 2024Review
- STAT6-targeting antisense oligonucleotides against solitary fibrous tumor.Molecular therapy. Nucleic acids · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Solitary fibrous tumor (SFT) is a rare soft-tissue sarcoma. This nonhereditary cancer is the result of an environmental intrachromosomal gene fusion between NAB2 and STAT6 on chromosome 12, which fuses the activation domain of STAT6 with the repression domain of NAB2. Currently there is not an approved chemotherapy regimen for SFTs. The best response on available pharmaceuticals is a partial response or stable disease for several months. The purpose of this study is to investigate the potential of RNA-based therapies for the treatment of SFTs. Specifically, in vitro SFT cell models were engineered to harbor the characteristic NAB2-STAT6 fusion using the CRISPR/SpCas9 system. Cell migration as well as multiple cancer-related signaling pathways were increased in the engineered cells as compared to the fusion-absent parent cells. The SFT cell models were then used for evaluating the targeting efficacies of NAB2-STAT6 fusion-specific antisense oligonucleotides (ASOs) and CRISPR/CasRx systems. Our results showed that fusion specific ASO treatments caused a 58% reduction in expression of fusion transcripts and a 22% reduction in cell proliferation after 72 h in vitro. Similarly, the AAV2-mediated CRISPR/CasRx system led to a 59% reduction in fusion transcript expressions in vitro, and a 55% reduction in xenograft growth after 29 days ex vivo.
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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.