ArticleNature communications2014
Extrachromosomal driver mutations in glioblastoma and low-grade glioma.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Reconstructing the molecular life history of gliomas.Acta neuropathologica · 2018Pooled it
- Extrachromosomal circular DNA: a potential clinical therapeutic target in malignant tumors.Cellular & molecular biology letters · 2026Review
- Article
- Periostin Safeguards EGFR-Driven Genomic Instability and Sustains the Immune-Suppressive Niche in Glioblastoma.Human mutation · 2026Article
- Extrachromosomal DNA in Solid Tumors-Landscape, Immune Effects, and Resistance to Targeted Therapy.Oncology research · 2026Review
- Extrachromosomal DNA-Driven Oncogene Spatial Heterogeneity and Evolution in Glioblastoma.Cancer discovery · 2025Article
- HyenaCircle: a HyenaDNA-based pretrained large language model for long eccDNA prediction.Frontiers in genetics · 2025Article
- Exploring the potential of extrachromosomal DNA as a novel oncogenic driver.Science China. Life sciences · 2025Review
- Repression of the SUMO-conjugating enzyme UBC9 is associated with lowered double minutes and reduced tumor progression.Cancer biology & therapy · 2024Article
- Article
- Multi-omics integration reveals the oncogenic role of eccDNAs in diffuse large B-cell lymphoma through STING signalling.Clinical and translational medicine · 2024Article
- Categorizing Extrachromosomal Circular DNA as Biomarkers in Serum of Cancer.Biomolecules · 2024Review
- Review
- Circular extrachromosomal DNA promotes tumor heterogeneity in high-risk medulloblastoma.Nature genetics · 2023Article
- Synthetic yeast chromosome XI design provides a testbed for the study of extrachromosomal circular DNA dynamics.Cell genomics · 2023Article
- Extrachromosomal circular DNA in colorectal cancer: biogenesis, function and potential as therapeutic target.Oncogene · 2023Review
- Unraveling the Impact of Intratumoral Heterogeneity on EGFR Tyrosine Kinase Inhibitor Resistance inInternational journal of molecular sciences · 2023Review
- Extrachromosomal DNA (ecDNA) in cancer: mechanisms, functions, and clinical implications.Frontiers in oncology · 2023Review
- Extrachromosomal DNA amplifications in cancer.Nature reviews. Genetics · 2022Review
- Uncovering novel mutational signatures byCell genomics · 2022Article
3 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
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Alteration of the number of copies of double minutes (DMs) with oncogenic EGFR mutations in response to tyrosine kinase inhibitors is a novel adaptive mechanism of glioblastoma. Here we provide evidence that such mutations in DMs, called here amplification-linked extrachromosomal mutations (ALEMs), originate extrachromosomally and could therefore be completely eliminated from the cancer cells. By exome sequencing of seven glioblastoma patients we reveal ALEMs in EGFR, PDGFRA and other genes. These mutations together with DMs are lost by cancer cells in culture. We confirm the extrachromosomal origin of such mutations by showing that wild-type and mutated DMs may coexist in the same tumour. Analysis of 4,198 tumours suggests the presence of ALEMs across different tumour types with the highest prevalence in glioblastomas and low-grade gliomas. The extrachromosomal nature of ALEMs explains the observed drastic changes in the amounts of mutated oncogenes (like EGFR or PDGFRA) in glioblastoma in response to environmental changes.
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.