ArticleNature genetics2018
Discordant inheritance of chromosomal and extrachromosomal DNA elements contributes to dynamic disease evolution in glioblastoma.
Article in Nature genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 2 of them syntheses that pooled it.
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
203 citing papers in PubMed, 2 syntheses or guidelines pooled it, 315 citations in OpenAlex.
- Temozolomide sensitivity of malignant glioma cell lines - a systematic review assessing consistencies between in vitro studies.BMC cancer · 2021Pooled it
- Reconstructing the molecular life history of gliomas.Acta neuropathologica · 2018Pooled it
- AmpliconSuite: an end-to-end workflow for analyzing focal amplifications in cancer genomes.Nature methods · 2026Article
- 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
- Extrachromosomal Circular DNA May Contribute to Histopathologic Characteristics in Esophageal Combined Basaloid Squamous Cell Carcinoma.Annals of surgical oncology · 2026Article
- Extrachromosomal DNA in urothelial carcinoma: mechanisms and clinical applications.Nature reviews. Urology · 2026Review
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Cis and trans regulatory mechanisms of extrachromosomal DNA segregation.Nature cell biology · 2026Article
- Extrachromosomal DNA Amplification as a Prognostic Factor for Cancer.Journal of personalized medicine · 2026Review
- Review
- Applications of transcranial focused ultrasound for primary brain tumors.Neuro-oncology advances · 2026Review
- lncRNA in EGFR‑driven glioblastoma.Nature cell biology · 2026Article
- Extrachromosomal DNA Gives Cancer a New Evolutionary Pathway.Research square · 2026Article
- Chromosome-arm-specific telomere length governs dual modes of structural genome evolution in IDH-mutant astrocytoma.bioRxiv : the preprint server for biology · 2026Article
- Functional role of small extrachromosomal circular DNA in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Plasma extrachromosomal circular DNA as a biomarker in EGFR-targeted therapy of non-small cell lung cancer.Molecular oncology · 2026Article
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- Article
- A novel CRISPR-Cas9 nickase-mediated rolling circle amplification (CRIRCA) technique for gene identification and quantitative analysis of extrachromosomal DNA.Journal of advanced research · 2026Article
143 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
19 authors at 6 institutions in 2 countries.
Funding
Abstract
To understand how genomic heterogeneity of glioblastoma (GBM) contributes to poor therapy response, we performed DNA and RNA sequencing on GBM samples and the neurospheres and orthotopic xenograft models derived from them. We used the resulting dataset to show that somatic driver alterations including single-nucleotide variants, focal DNA alterations and oncogene amplification on extrachromosomal DNA (ecDNA) elements were in majority propagated from tumor to model systems. In several instances, ecDNAs and chromosomal alterations demonstrated divergent inheritance patterns and clonal selection dynamics during cell culture and xenografting. We infer that ecDNA was unevenly inherited by offspring cells, a characteristic that affects the oncogenic potential of cells with more or fewer ecDNAs. Longitudinal patient tumor profiling found that oncogenic ecDNAs are frequently retained throughout the course of disease. Our analysis shows that extrachromosomal elements allow rapid increase of genomic heterogeneity during GBM evolution, independently of chromosomal DNA alterations.
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.