ReviewCell research2025
Modern biology of extrachromosomal DNA: A decade-long voyage of discovery.
Review in Cell research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed.
- Cryo-EM structure of a 95-base-pair double-stranded DNA minicircle at 5.3 Å resolution.Nucleic acids research · 2026Article
- Extrachromosomal DNA in urothelial carcinoma: mechanisms and clinical applications.Nature reviews. Urology · 2026Review
- Hybrid extrachromosomal DNA in HPV-driven cancers.Journal of virology · 2026Review
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Cis and trans regulatory mechanisms of extrachromosomal DNA segregation.Nature cell biology · 2026Article
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- The newfound relationship between extrachromosomal DNAs and excised signal circles.FEBS letters · 2026Review
- Targeting extrachromosomal DNA in human cancers.Nature reviews. Drug discovery · 2026Review
- TONSOKU prevents the formation of large tandem duplications and restrains ATR-WEE1 checkpoint activation.Nature communications · 2026Article
- Article
- Extrachromosomal DNA and cancer: function, formation, and clinical implications.Journal of experimental & clinical cancer research : CR · 2026Review
- The Extrachromosomal DNA Fusion Factory: Extrachromosomal Genesis of Oncogenic Fusion Transcripts.Research (Washington, D.C.) · 2026Article
- BRIGHT Enables High-SNR Live-Cell Imaging of Non-Repetitive Sequences via Bivalent Fluorescent Nanobody-Mediated Cascade-Dependent Illumination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Innate immune sensing via the cGAS-STING pathway restricts extrachromosomal DNA-driven tumorigenesis.bioRxiv : the preprint server for biology · 2026Article
- Extrachromosomal DNA in Solid Tumors-Landscape, Immune Effects, and Resistance to Targeted Therapy.Oncology research · 2026Review
- Selective genome editing of amplified oncogenes triggers immunogenic cell death and tumor remodeling.Molecular cancer · 2025Article
- ecDNA-driven oncogene super-expressors shape immunoevasive tumor microenvironment.bioRxiv : the preprint server for biology · 2025Article
- DNA damage response pathway is a promising therapeutic target for extrachromosomal DNA-positive tumours.Clinical and translational medicine · 2025Article
- Nucleic Acid Diversity in cGAS-STING Pathway Activation and Immune Dysregulation.Biomedicines · 2025Review
- Interferon Epsilon Loss Is Elusive 9p21 Link to Immune-Cold Tumors, Resistant to Immune Checkpoint Therapy, and Endogenous CXCL9/10 Induction.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Genomic instability is a hallmark of cancer and is a major driving force of tumorigenesis. A key manifestation of genomic instability is the formation of extrachromosomal DNAs (ecDNAs) - acentric, circular DNA molecules ranging from 50 kb to 5 Mb in size, distinct from chromosomes. Ontological studies have revealed that ecDNA serves as a carrier of oncogenes, immunoregulatory genes, and enhancers, capable of driving elevated transcription of its cargo genes and cancer heterogeneity, leading to rapid tumor evolution and therapy resistance. Although ecDNA was documented over half a century ago, the past decade has witnessed a surge in breakthrough discoveries about its biological functions. Here, we systematically review the modern biology of ecDNA uncovered over the last ten years, focusing on how discoveries during this pioneering stage have illuminated our understanding of ecDNA-driven transcription, heterogeneity, and cancer progression. Furthermore, we discuss ongoing efforts to target ecDNA as a novel approach to cancer therapy. This burgeoning field is entering a new phase, poised to reshape our knowledge of cancer biology and therapeutic strategies.
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What Socratic 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 Socratic graph.