ArticlePloS one2008
Binomial mitotic segregation of MYCN-carrying double minutes in neuroblastoma illustrates the role of randomness in oncogene amplification.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 49 citations in OpenAlex.
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- Genetic elements promote retention of extrachromosomal DNA in cancer cells.bioRxiv : the preprint server for biology · 2025Article
- Modern biology of extrachromosomal DNA: A decade-long voyage of discovery.Cell research · 2025Review
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- Imaging extrachromosomal DNA (ecDNA) in cancer.Histochemistry and cell biology · 2024Review
- Categorizing Extrachromosomal Circular DNA as Biomarkers in Serum of Cancer.Biomolecules · 2024Review
- Extrachromosomal Circular DNA: An Emerging Potential Biomarker for Inflammatory Bowel Diseases?Genes · 2024Review
- EccBase: A high-quality database for exploration and characterization of extrachromosomal circular DNAs in cancer.Computational and structural biotechnology journal · 2023Article
- Extrachromosomal DNA amplifications in cancer.Nature reviews. Genetics · 2022Review
- Leveraging extrachromosomal DNA to fine-tune trials of targeted therapy for glioblastoma: opportunities and challenges.Nature reviews. Clinical oncology · 2022Review
- Extrachromosomal circular DNA: biogenesis, structure, functions and diseases.Signal transduction and targeted therapy · 2022Review
- Extrachromosomal DNA in Cancer.Annual review of genomics and human genetics · 2022Review
- Gene regulation on extrachromosomal DNA.Nature structural & molecular biology · 2022Review
- Plasticity of Extrachromosomal and Intrachromosomal BRAF Amplifications in Overcoming Targeted Therapy Dosage Challenges.Cancer discovery · 2022Article
- Live-Cell Imaging Shows Uneven Segregation of Extrachromosomal DNA Elements and Transcriptionally Active Extrachromosomal DNA Hubs in Cancer.Cancer discovery · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmplification of the oncogene MYCN in double minutes (DMs) is a common finding in neuroblastoma (NB). Because DMs lack centromeric sequences it has been unclear how NB cells retain and amplify extrachromosomal MYCN copies during tumour development. PRINCIPAL
findingsWe show that MYCN-carrying DMs in NB cells translocate from the nuclear interior to the periphery of the condensing chromatin at transition from interphase to prophase and are preferentially located adjacent to the telomere repeat sequences of the chromosomes throughout cell division. However, DM segregation was not affected by disruption of the telosome nucleoprotein complex and DMs readily migrated from human to murine chromatin in human/mouse cell hybrids, indicating that they do not bind to specific positional elements in human chromosomes. Scoring DM copy-numbers in ana/telophase cells revealed that DM segregation could be closely approximated by a binomial random distribution. Colony-forming assay demonstrated a strong growth-advantage for NB cells with high DM (MYCN) copy-numbers, compared to NB cells with lower copy-numbers. In fact, the overall distribution of DMs in growing NB cell populations could be readily reproduced by a mathematical model assuming binomial segregation at cell division combined with a proliferative advantage for cells with high DM copy-numbers.
conclusionBinomial segregation at cell division explains the high degree of MYCN copy-number variability in NB. Our findings also provide a proof-of-principle for oncogene amplification through creation of genetic diversity by random events followed by Darwinian selection.
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