ArticleNucleic acids research2014
Genomic organization and evolution of double minutes/homogeneously staining regions with MYC amplification in human cancer.
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 76 papers.
What it found
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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.
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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.
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Who cites it
76 citing papers in PubMed, 108 citations in OpenAlex.
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- Homovanillic acid and vanillylmandelic acid as neuroblastoma biomarkers in children.Biochemia medica · 2026Review
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
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- Genetic and chromosomal dysregulations of progenitor cells in the etiology and pathogenesis of pediatric cancers.American journal of stem cells · 2026Review
- Tailorable porous collagen hydrogels as a physiologically relevant platform for extrachromosomal DNA-associated colorectal cancer research.Theranostics · 2026Article
- The Occurrence of Gene Fusions in Thyroid Lesions and the Relation With Chronic Lymphocytic Thyroiditis.Pathology international · 2026Article
- Extrachromosomal DNA: shaping the evolutionary dynamics of cancer.Trends in cancer · 2025Review
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- Synergistic RAS-MAPK and AKT Activation in MYC-Driven Tumors via Adjacent PVT1 Rearrangements.bioRxiv : the preprint server for biology · 2025Article
- Extrachromosomal circular DNA: a double-edged sword in cancer progression and age-related diseases.Human cell · 2025Review
- The role of extrachromosomal DNA in tumorigenesis and progression.Frontiers in oncology · 2025Review
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
- Article
- Chromothripsis: an emerging crossroad from aberrant mitosis to therapeutic opportunities.Journal of molecular cell biology · 2024Review
- Categorizing Extrachromosomal Circular DNA as Biomarkers in Serum of Cancer.Biomolecules · 2024Review
- Extrachromosomal DNA in cancer.Nature reviews. Cancer · 2024Review
- Review
- Advancements in Focal Amplification Detection in Tumor/Liquid Biopsies and Emerging Clinical Applications.Genes · 2023Review
- Extrachromosomal circular DNA in colorectal cancer: biogenesis, function and potential as therapeutic target.Oncogene · 2023Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 7 institutions in 4 countries.
Funding
Abstract
The mechanism for generating double minutes chromosomes (dmin) and homogeneously staining regions (hsr) in cancer is still poorly understood. Through an integrated approach combining next-generation sequencing, single nucleotide polymorphism array, fluorescent in situ hybridization and polymerase chain reaction-based techniques, we inferred the fine structure of MYC-containing dmin/hsr amplicons harboring sequences from several different chromosomes in seven tumor cell lines, and characterized an unprecedented number of hsr insertion sites. Local chromosome shattering involving a single-step catastrophic event (chromothripsis) was recently proposed to explain clustered chromosomal rearrangements and genomic amplifications in cancer. Our bioinformatics analyses based on the listed criteria to define chromothripsis led us to exclude it as the driving force underlying amplicon genesis in our samples. Instead, the finding of coexisting heterogeneous amplicons, differing in their complexity and chromosome content, in cell lines derived from the same tumor indicated the occurrence of a multi-step evolutionary process in the genesis of dmin/hsr. Our integrated approach allowed us to gather a complete view of the complex chromosome rearrangements occurring within MYC amplicons, suggesting that more than one model may be invoked to explain the origin of dmin/hsr in cancer. Finally, we identified PVT1 as a target of fusion events, confirming its role as breakpoint hotspot in MYC amplification.
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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.