ArticleNature communications2025
Breakage fusion bridge cycles drive high oncogene number with moderate intratumoural heterogeneity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.Annals of medicine · 2026Review
- STK11 Mutations and Deletions Define an Aggressive Molecular Subgroup of Cervical Adenocarcinoma.Cancer medicine · 2026Article
- scAmp enables focal gene amplification analysis from single-cell data.Nature communications · 2026Article
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Detecting and reconstructing breakage-fusion-bridge cycles from long-read sequencing using BFBArchitect.Bioinformatics (Oxford, England) · 2026Article
- Targeting extrachromosomal DNA in human cancers.Nature reviews. Drug discovery · 2026Review
- Review
- Fast and accurate resolution of ecDNA sequence using Cycle-Extractor.bioRxiv : the preprint server for biology · 2026Article
- Convergent evolution of complex structural variants drives therapy resistance in metastatic prostate cancer.Genome biology · 2026Article
- Accurate prediction of ecDNA in interphase cancer cells using deep neural networks.Communications biology · 2026Article
- scAmp analyzes focal gene amplifications at single-cell resolution.bioRxiv : the preprint server for biology · 2026Article
- Cross-Species Exome Sequencing Reveals Recurrent Genomic Alterations in California Sea Lion (Genes · 2026Article
- Article
- Selective genome editing of amplified oncogenes triggers immunogenic cell death and tumor remodeling.Molecular cancer · 2025Article
- Megabase-scale loss of heterozygosity provoked by CRISPR-Cas9 DNA double-strand breaks.Molecular cell · 2025Article
- Aqueous Humor Liquid Biopsy Identifies Murine Double Minute 4 Segmental Gain in Retinoblastoma: Implications for Chemotherapy Response and Precision Oncology.JCO precision oncology · 2025Article
- A Guide to Extrachromosomal DNA: Cancer's Dynamic Circular Genome.Cancer discovery · 2025Review
- Breakage fusion bridge cycles drive high oncogene number with moderate intratumoural heterogeneity.Nature communications · 2025Article
- The role of extrachromosomal DNA in tumorigenesis and progression.Frontiers in oncology · 2025Review
Corrections and comments
- Update of
Authors and funding
30 authors.
Funding
Abstract
Oncogene amplification is a key driver of cancer pathogenesis. Both breakage fusion bridge (BFB) cycles and extrachromosomal DNA (ecDNA) can lead to high oncogene copy numbers, but the impact of BFB amplifications on intratumoral heterogeneity, treatment response, and patient survival remains poorly understood due to detection challenges with DNA sequencing. We introduce an algorithm, OM2BFB, designed to detect and reconstruct BFB amplifications using optical genome mapping (OGM). OM2BFB demonstrates high precision (>93%) and recall (92%) in identifying BFB amplifications across cancer cell lines, patient-derived xenograft models, and primary tumors. Comparisons using OGM reveal that BFB detection with our AmpliconSuite toolkit for short-read sequencing also achieves high precision, though with reduced sensitivity. We identify 371 BFB events through whole genome sequencing of 2557 primary tumors and cancer cell lines. BFB amplifications are prevalent in cervical, head and neck, lung, and esophageal cancers, but rare in brain cancers. Genes amplified through BFB exhibit lower expression variance, with limited potential for regulatory adaptation compared to ecDNA-amplified genes. Tumors with BFB amplifications (BFB(+)) show reduced structural heterogeneity in amplicons and delayed resistance onset relative to ecDNA(+) tumors. These findings highlight ecDNA and BFB amplifications as distinct oncogene amplification mechanisms with differing biological characteristics, suggesting distinct avenues for therapeutic intervention.
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.