ArticleScience (New York, N.Y.)2020
Mechanisms generating cancer genome complexity from a single cell division error.
Article in Science (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 267 papers.
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Who cites it
267 citing papers in PubMed.
- Atypical fusion among non-malignant cells: Unveiling the link between post-fusion-induced genome chaos and cancer initiation.Cancer cell international · 2026Article
- Micronuclear ecDNA constrains tumor cell fitness and is associated with favorable patient survival.Nature genetics · 2026Article
- Circular DNA exposes a weakness in cancer cells.Nature · 2026Article
- A protective ESCRT sleeve for ultrafine DNA bridges.Nature structural & molecular biology · 2026Article
- ESCRT-III assembles around mis-segregated DNA to protect genome stability.Nature structural & molecular biology · 2026Article
- Article
- A single chromosome 3p break initiates clear cell renal cell carcinoma evolution.bioRxiv : the preprint server for biology · 2026Article
- Detecting and reconstructing breakage-fusion-bridge cycles from long-read sequencing using BFBArchitect.Bioinformatics (Oxford, England) · 2026Article
- Deciphering mitotic catastrophe-associated transcriptomic patterns in renal cell carcinoma: prognostic significance and immunotherapy-related associations.Biology direct · 2026Article
- Enhanced genetic diagnosis in early pregnancy loss: an integrated approach using CNV-Seq and STR genotyping.Reproductive biology and endocrinology : RB&E · 2026Article
- Telomere Dysfunction in Human Astrocytes Drives Acrocentric Chromosome Instability and Nucleolar Reorganization.bioRxiv : the preprint server for biology · 2026Article
- Simultaneous CRISPR/Cas9-induced double-strand breaks are lethal in models of pancreatic cancer.The Journal of clinical investigation · 2026Article
- Lesions initiating spontaneous mitotic crossover are minimally subject to non-homologous end joining.bioRxiv : the preprint server for biology · 2026Article
- The landscape of structural variation in pediatric cancer.Cancer cell · 2026Article
- Chromosome-arm-specific telomere length governs dual modes of structural genome evolution in IDH-mutant astrocytoma.bioRxiv : the preprint server for biology · 2026Article
- Recurrent DNA break clusters drive replication-stress-induced copy number variants and genome diversification.Nature communications · 2026Article
- Review
- Integrative Multi-Omics Analysis Reveals HNRNPLL as a Potential Biomarker Associated with Hepatocellular Carcinoma Progression.Metabolites · 2026Article
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- Haplotype-resolved reconstruction and functional interrogation of cancer karyotypes.Cell systems · 2026Article
207 more citing papers are in PubMed but not listed here.
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12 authors.
Funding
Abstract
The chromosome breakage-fusion-bridge (BFB) cycle is a mutational process that produces gene amplification and genome instability. Signatures of BFB cycles can be observed in cancer genomes alongside chromothripsis, another catastrophic mutational phenomenon. We explain this association by elucidating a mutational cascade that is triggered by a single cell division error-chromosome bridge formation-that rapidly increases genomic complexity. We show that actomyosin forces are required for initial bridge breakage. Chromothripsis accumulates, beginning with aberrant interphase replication of bridge DNA. A subsequent burst of DNA replication in the next mitosis generates extensive DNA damage. During this second cell division, broken bridge chromosomes frequently missegregate and form micronuclei, promoting additional chromothripsis. We propose that iterations of this mutational cascade generate the continuing evolution and subclonal heterogeneity characteristic of many human cancers.
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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.