ArticleGenome research2010
Gene amplification as double minutes or homogeneously staining regions in solid tumors: origin and structure.
Article in Genome research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.
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
150 citing papers in PubMed, 1 synthesis or guideline pooled it, 255 citations in OpenAlex.
- Characterization, biogenesis model, and current bioinformatics of human extrachromosomal circular DNA.Frontiers in genetics · 2024Pooled it
- A Living Multi-Omics PDX Biobank of High-Risk Sarcomas Reveals ecDNA-Driven Oncogene Amplification in Osteosarcoma and Enables Preclinical Precision Oncology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Quantitative and sensitive neuroblastoma minimal residual disease detection using extrachromosomal DNA (ecDNA) breakpoints.bioRxiv : the preprint server for biology · 2026Article
- Integrating molecular subtypes, genomics and functional dependencies to identify context-specific therapeutic vulnerabilities in small cell lung cancer.Biomarker research · 2026Review
- Review
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- Optimized CRISPR-Cas9 system for efficient engineering of ecDNA in cancer cells.Nucleic acids research · 2026Article
- Clinicopathological and genomic features of extrachromosomal DNA in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Article
- Selective genome editing of amplified oncogenes triggers immunogenic cell death and tumor remodeling.Molecular cancer · 2025Article
- cfOncoXpress: Tumor gene expression prediction from cell-free DNA whole-genome sequences.bioRxiv : the preprint server for biology · 2025Article
- Extrachromosomal DNA-Driven Oncogene Dosage Heterogeneity Promotes Rapid Adaptation to Therapy in MYCN-Amplified Cancers.Cancer discovery · 2025Article
- Panorama of Chromosomal Instability in Lung Cancer.medRxiv : the preprint server for health sciences · 2025Article
- A Guide to Extrachromosomal DNA: Cancer's Dynamic Circular Genome.Cancer discovery · 2025Review
- Disparate Pathways for Extrachromosomal DNA Biogenesis and Genomic DNA Repair.Cancer discovery · 2025Article
- Exploring the potential of extrachromosomal DNA as a novel oncogenic driver.Science China. Life sciences · 2025Review
- Integrated CIRCLE-seq with RNA-seq to decipher the quantity, localization, and functional features of eccDNA in AML.Frontiers in oncology · 2025Article
- Extrachromosomal circular DNA and their roles in cancer progression.Genes & diseases · 2025Review
- Repression of the SUMO-conjugating enzyme UBC9 is associated with lowered double minutes and reduced tumor progression.Cancer biology & therapy · 2024Article
- Unveiling the mysteries of extrachromosomal circular DNA: from generation to clinical relevance in human cancers and health.Molecular cancer · 2024Review
90 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
16 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double minutes (dmin) and homogeneously staining regions (hsr) are the cytogenetic hallmarks of genomic amplification in cancer. Different mechanisms have been proposed to explain their genesis. Recently, our group showed that the MYC-containing dmin in leukemia cases arise by excision and amplification (episome model). In the present paper we investigated 10 cell lines from solid tumors showing MYCN amplification as dmin or hsr. Particularly revealing results were provided by the two subclones of the neuroblastoma cell line STA-NB-10, one showing dmin-only and the second hsr-only amplification. Both subclones showed a deletion, at 2p24.3, whose extension matched the amplicon extension. Additionally, the amplicon structure of the dmin and hsr forms was identical. This strongly argues that the episome model, already demonstrated in leukemias, applies to solid tumors as well, and that dmin and hsr are two faces of the same coin. The organization of the duplicated segments varied from very simple (no apparent changes from the normal sequence) to very complex. MYCN was always overexpressed (significantly overexpressed in three cases). The fusion junctions, always mediated by nonhomologous end joining, occasionally juxtaposed truncated genes in the same transcriptional orientation. Fusion transcripts involving NBAS (also known as NAG), FAM49A, BC035112 (also known as NCRNA00276), and SMC6 genes were indeed detected, although their role in the context of the tumor is not clear.
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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.