ArticleNature communications2023
Etiology of oncogenic fusions in 5,190 childhood cancers and its clinical and therapeutic implication.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Cancer-associated fusion transcripts: mechanisms, functional roles, and clinical implications.Clinical and experimental medicine · 2026Review
- Pediatric sarcomas: challenges and opportunities.Genes & development · 2026Review
- Single-cell multi-omic analyses resolve the cellular diversity of ALK/ROS1/MET/NTRK-fused gliomas in infants and older children.bioRxiv : the preprint server for biology · 2026Article
- TCF3::HLF-positive B-ALL: integrated clinical and molecular characterization of 34 cases from a single-center cohort.British journal of cancer · 2026Article
- Advances in targeted therapies for pediatric tumors.Acta pharmacologica Sinica · 2026Article
- Review
- Molecular risk markers define risk of relapse in myeloid leukemia of Down syndrome beyond measurable residual disease.Blood advances · 2026Article
- The GF-NEO discovery platform unveils a [KQE][DG] sequence motif within fusion neoantigens in pediatric cancer.iScience · 2026Article
- Analysis of error profiles of indels and structural variants in deep-sequencing data.Cell genomics · 2026Article
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- CanID: A Robust and Accurate RNA-seq Expression-based Diagnostic Classification Scheme for Pediatric Malignancies.Genomics, proteomics & bioinformatics · 2025Article
- Fast and sensitive detection of targeted gene fusions using frequency minimizers and fuzzy pattern matching with Fuzzion2.Cell reports methods · 2025Article
- Rewiring the Fusion Oncoprotein EWSR1::FLI1 in Ewing Sarcoma with Bivalent Small Molecules.Journal of the American Chemical Society · 2025Article
- Article
- Qingre Huoxue decoction and its active compound Quercetin modulate bone remodeling by inhibiting ATF4 hyperactivation to attenuate bone erosion in rheumatoid arthritis.Journal of orthopaedic surgery and research · 2025Article
- Clinical utility of targeted RNA sequencing in cancer molecular diagnostics.Nature medicine · 2025Article
- The power of RNA sequencing in molecular oncology.Nature medicine · 2025Article
- Massively parallel immunopeptidome by DNA sequencing provides insights into cancer antigen presentation.Nature genetics · 2025Article
- Clinical Implementation of Expanded Solid Tumor Fusion Detection With Whole-Transcriptome Sequencing at an Academic Cancer Center.JCO precision oncology · 2025Article
- Rapid and robust validation of pooled CRISPR knockout screens using CelFi.Scientific reports · 2025Article
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Authors and funding
33 authors at 9 institutions in 4 countries.
Funding
Abstract
Oncogenic fusions formed through chromosomal rearrangements are hallmarks of childhood cancer that define cancer subtype, predict outcome, persist through treatment, and can be ideal therapeutic targets. However, mechanistic understanding of the etiology of oncogenic fusions remains elusive. Here we report a comprehensive detection of 272 oncogenic fusion gene pairs by using tumor transcriptome sequencing data from 5190 childhood cancer patients. We identify diverse factors, including translation frame, protein domain, splicing, and gene length, that shape the formation of oncogenic fusions. Our mathematical modeling reveals a strong link between differential selection pressure and clinical outcome in CBFB-MYH11. We discover 4 oncogenic fusions, including RUNX1-RUNX1T1, TCF3-PBX1, CBFA2T3-GLIS2, and KMT2A-AFDN, with promoter-hijacking-like features that may offer alternative strategies for therapeutic targeting. We uncover extensive alternative splicing in oncogenic fusions including KMT2A-MLLT3, KMT2A-MLLT10, C11orf95-RELA, NUP98-NSD1, KMT2A-AFDN and ETV6-RUNX1. We discover neo splice sites in 18 oncogenic fusion gene pairs and demonstrate that such splice sites confer therapeutic vulnerability for etiology-based genome editing. Our study reveals general principles on the etiology of oncogenic fusions in childhood cancer and suggests profound clinical implications including etiology-based risk stratification and genome-editing-based therapeutics.
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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.