ArticleJournal of mathematical biology2016
Modeling the evolution space of breakage fusion bridge cycles with a stochastic folding process.
Article in Journal of mathematical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The newfound relationship between extrachromosomal DNAs and excised signal circles.FEBS letters · 2026Review
- Breakage fusion bridge cycles drive high oncogene number with moderate intratumoural heterogeneity.Nature communications · 2025Article
- Breakage fusion bridge cycles drive high oncogene copy number, but not intratumoral genetic heterogeneity or rapid cancer genome change.bioRxiv : the preprint server for biology · 2023Article
- Deciphering complex breakage-fusion-bridge genome rearrangements with Ambigram.Nature communications · 2023Article
- Integrated Genomic, Epigenomic, and Expression Analyses of Ovarian Cancer Cell Lines.Cell reports · 2018Article
- Patterns and mechanisms of structural variations in human cancer.Experimental & molecular medicine · 2018Review
- Modeling cancer rearrangement landscapes.Current opinion in systems biology · 2017Article
- A whole-genome sequence and transcriptome perspective on HER2-positive breast cancers.Nature communications · 2016Article
- Disease evolution and heterogeneity in bilateral breast cancer.American journal of cancer research · 2016Article
- Reconstructing breakage fusion bridge architectures using noisy copy numbers.Journal of computational biology : a journal of computational molecular cell biology · 2015Article
- Chromothripsis and beyond: rapid genome evolution from complex chromosomal rearrangements.Genes & development · 2013Review
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Authors and funding
5 authors.
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Abstract
Breakage-fusion-bridge cycles in cancer arise when a broken segment of DNA is duplicated and an end from each copy joined together. This structure then 'unfolds' into a new piece of palindromic DNA. This is one mechanism responsible for the localised amplicons observed in cancer genome data. Here we study the evolution space of breakage-fusion-bridge structures in detail. We firstly consider discrete representations of this space with 2-d trees to demonstrate that there are [Formula: see text] qualitatively distinct evolutions involving [Formula: see text] breakage-fusion-bridge cycles. Secondly we consider the stochastic nature of the process to show these evolutions are not equally likely, and also describe how amplicons become localized. Finally we highlight these methods by inferring the evolution of breakage-fusion-bridge cycles with data from primary tissue cancer samples.
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