ArticleNature communications2024
EWS-WT1 fusion isoforms establish oncogenic programs and therapeutic vulnerabilities in desmoplastic small round cell tumors.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Evaluation of novel targeted small-molecule therapeutics in desmoplastic small round cell tumor (DSRCT) cells.Journal of cancer research and clinical oncology · 2026Article
- Review
- Harnessing AACR Project GENIE to Define the Molecular Features of Desmoplastic Small Round Cell Tumor.Current issues in molecular biology · 2026Article
- Review
- EWS::WT1 Isoform-Dependent Regulation of Neogenes in Desmoplastic Small Round Cell Tumors.bioRxiv : the preprint server for biology · 2025Article
- Desmoplastic Small Round Cell Tumors and the Role of Androgen Receptors.Current treatment options in oncology · 2025Review
- Comprehensive DSRCT multi-omics analyses unveil CACNA2D2 as a diagnostic hallmark and super-enhancer-driven EWSR1::WT1 signature gene.Cancer communications (London, England) · 2025Article
- Desmoplastic small round cell tumor: an update of current management practices.Journal of the Egyptian National Cancer Institute · 2025Review
- High expression level of ERBB2 and efficacy of trastuzumab deruxtecan in desmoplastic small round cell tumour: a monocentric case series report.ESMO open · 2025Article
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
EWS fusion oncoproteins underlie several human malignancies including Desmoplastic Small Round Cell Tumor (DSRCT), an aggressive cancer driven by EWS-WT1 fusion proteins. Here we combine chromatin occupancy and 3D profiles to identify EWS-WT1-dependent gene regulation networks and target genes. We show that EWS-WT1 is a powerful chromatin activator controlling an oncogenic gene expression program that characterizes primary tumors. Similar to wild type WT1, EWS-WT1 has two isoforms that differ in their DNA binding domain and we find that they have distinct DNA binding profiles and are both required to generate viable tumors that resemble primary DSRCT. Finally, we identify candidate EWS-WT1 target genes with potential therapeutic implications, including CCND1, whose inhibition by the clinically-approved drug Palbociclib leads to marked tumor burden decrease in DSRCT PDXs in vivo. Taken together, our studies identify gene regulation programs and therapeutic vulnerabilities in DSRCT and provide a mechanistic understanding of the complex oncogenic activity of EWS-WT1.
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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.