ArticleCancers2021
Therapeutic Potential of
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
22 citing papers in PubMed, 25 citations in OpenAlex.
- Immunotherapy in pediatric bone sarcomas: Current progress and future directions.Human vaccines & immunotherapeutics · 2026Review
- FusionTarget: Computational framework for drug repurposing against modeled fusion protein structures from genomic breakpoints.iScience · 2026Article
- Liquid biopsy in malignant primary bone tumors: Clinical applications of circulating tumor DNA and circulating tumor cells for diagnosis, prognosis and treatment monitoring (Review).Oncology reports · 2026Review
- Suppressing the Aberrant Transcriptional Functionality of EWS::FLI1 Oncoprotein by Designer polyQ Fusions with Its Homologous Peptides.Biomedicines · 2026Article
- Targeting oncogenic fusion-driven NUT carcinoma with CRISPR-Cas9 genome editing.Molecular therapy. Oncology · 2025Article
- Fusion genes in cancers: Biogenesis, functions, and therapeutic implications.Genes & diseases · 2025Review
- Suicide gene therapy targeting ewing sarcoma via an ewing-specific GGAA promoter.Scientific reports · 2025Article
- Targeted inactivation of EWSR1 : : FLI1 gene in Ewing sarcoma via CRISPR/Cas9 driven by an Ewing-specific GGAA promoter.Cancer gene therapy · 2025Article
- CRISPR/Cas9 technology in tumor research and drug development application progress and future prospects.Frontiers in pharmacology · 2025Review
- A comprehensive overview of liquid biopsy applications in pediatric solid tumors.NPJ precision oncology · 2024Review
- Ewing sarcoma of the cervix: an unusual site of presentation.BMJ case reports · 2024Article
- Ewing sarcoma treatment: a gene therapy approach.Cancer gene therapy · 2023Review
- An unusual presentation of extraskeletal vaginal Ewing sarcoma: A case report.Case reports in women's health · 2023Article
- Prospects and Advances in Adoptive Natural Killer Cell Therapy for Unmet Therapeutic Needs in Pediatric Bone Sarcomas.International journal of molecular sciences · 2023Review
- Evolution of CRISPR-associated endonucleases as inferred from resurrected proteins.Nature microbiology · 2023Article
- Specific correction of pyruvate kinase deficiency-causing point mutations by CRISPR/Cas9 and single-stranded oligodeoxynucleotides.Frontiers in genome editing · 2023Article
- Ten Years of CRISPRing Cancers In Vitro.Cancers · 2022Review
- Review
- Establishment and characterization of a novel patient-derived Ewing sarcoma cell line, NCC-ES2-C1.Human cell · 2022Article
- Epigenetic and Transcriptional Signaling in Ewing Sarcoma-Disease Etiology and Therapeutic Opportunities.Biomedicines · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Ewing sarcoma is an aggressive bone cancer affecting children and young adults. The main molecular hallmark of Ewing sarcoma are chromosomal translocations that produce chimeric oncogenic transcription factors, the most frequent of which is the aberrant transcription factor EWSR1-FLI1. Because this is the principal oncogenic driver of Ewing sarcoma, its inactivation should be the best therapeutic strategy to block tumor growth. In this study, we genetically inactivated EWSR1-FLI1 using CRISPR-Cas9 technology in order to cause permanent gene inactivation. We found that gene editing at the exon 9 of FLI1 was able to block cell proliferation drastically and induce senescence massively in the well-studied Ewing sarcoma cell line A673. In comparison with an extensively used cellular model of EWSR1-FLI1 knockdown (A673/TR/shEF), genetic inactivation was more effective, particularly in its capability to block cell proliferation. In summary, genetic inactivation of EWSR1-FLI1 in A673 Ewing sarcoma cells blocks cell proliferation and induces a senescence phenotype that could be exploited therapeutically. Although efficient and specific in vivo CRISPR-Cas9 editing still presents many challenges today, our data suggest that complete inactivation of EWSR1-FLI1 at the cell level should be considered a therapeutic approach to develop in the future.
Indexed as
Identifiers
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.