ArticleNucleic acids research2014
Amplicon rearrangements during the extrachromosomal and intrachromosomal amplification process in a glioma.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 56 citations in OpenAlex.
- Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.Genome research · 2026Article
- Dysfunctional DNA Mismatch Repair Drives the Evolution of Gene Amplification in MTX-Resistant Human Colorectal Cancer Cells.International journal of molecular sciences · 2026Article
- DeepECC: a deep learning framework for genome-wide identification and analysis of human cancer eccDNAs.Nucleic acids research · 2026Article
- Circulating Cell-free DNA Fragmentomics Detection and Beyond.Aging and disease · 2025Review
- Review
- Intercellular extrachromosomal DNA copy-number heterogeneity drives neuroblastoma cell state diversity.Cell reports · 2024Article
- Multi-omics integration reveals the oncogenic role of eccDNAs in diffuse large B-cell lymphoma through STING signalling.Clinical and translational medicine · 2024Article
- Beyond the Chromosome: Recent Developments in Decoding the Significance of Extrachromosomal Circular DNA (eccDNA) in Human Malignancies.Life (Basel, Switzerland) · 2024Review
- Review
- Extrachromosomal Circular DNA: An Emerging Potential Biomarker for Inflammatory Bowel Diseases?Genes · 2024Review
- 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
- Life of double minutes: generation, maintenance, and elimination.Chromosoma · 2022Review
- Extrachromosomal DNA in Cancer.Annual review of genomics and human genetics · 2022Review
- Revisiting characteristics of oncogenic extrachromosomal DNA as mobile enhancers on neuroblastoma and glioma cancers.Cancer cell international · 2022Review
- Revisiting chemoresistance in ovarian cancer: Mechanism, biomarkers, and precision medicine.Genes & diseases · 2022Review
- Global characterization of extrachromosomal circular DNAs in advanced high grade serous ovarian cancer.Cell death & disease · 2022Article
- Extrachromosomal DNA: An Emerging Hallmark in Human Cancer.Annual review of pathology · 2022Review
- Pioneering insights of extrachromosomal DNA (ecDNA) generation, action and its implications for cancer therapy.International journal of biological sciences · 2022Review
- Extrachromosomal Circular DNA: A New Target in Cancer.Frontiers in oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms of gene amplification in tumour cells are poorly understood and the relationship between extrachromosomal DNA molecules, named double minutes (dmins), and intrachromosomal homogeneously staining regions (hsr) is not documented at nucleotide resolution. Using fluorescent in situ hybridization and whole genome sequencing, we studied a xenografted human oligodendroglioma where the co-amplification of the EGFR and MYC loci was present in the form of dmins at early passages and of an hsr at later passages. The amplified regions underwent multiple rearrangements and deletions during the formation of the dmins and their transformation into hsr. In both forms of amplification, non-homologous end-joining and microhomology-mediated end-joining rather than replication repair mechanisms prevailed in fusions. Small fragments, some of a few tens of base pairs, were associated in contigs. They came from clusters of breakpoints localized hundreds of kilobases apart in the amplified regions. The characteristics of some pairs of junctions suggest that at least some fragments were not fused randomly but could result from the concomitant repair of neighbouring breakpoints during the interaction of remote DNA sequences. This characterization at nucleotide resolution of the transition between extra- and intrachromosome amplifications highlights a hitherto uncharacterized organization of the amplified regions suggesting the involvement of new mechanisms in their formation.
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.