ArticleScientific reports2015
Double minute amplification of mutant PDGF receptor α in a mouse glioma model.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Disrupting PDGFRA-driven immune evasion in glioma: vaccine-based strategies on the horizon.Frontiers in oncology · 2026Review
- Article
- Leveraging extrachromosomal DNA to fine-tune trials of targeted therapy for glioblastoma: opportunities and challenges.Nature reviews. Clinical oncology · 2022Review
- EPHA2 mediates PDGFA activity and functions together with PDGFRA as prognostic marker and therapeutic target in glioblastoma.Signal transduction and targeted therapy · 2022Article
- Receptor tyrosine kinase (RTK) targeting in pediatric high-grade glioma and diffuse midline glioma: Pre-clinical models and precision medicine.Frontiers in oncology · 2022Review
- Current understanding of extrachromosomal circular DNA in cancer pathogenesis and therapeutic resistance.Journal of hematology & oncology · 2020Review
- Longitudinal assessment of tumor development using cancer avatars derived from genetically engineered pluripotent stem cells.Nature communications · 2020Article
- New insights of extrachromosomal DNA in tumorigenesis and therapeutic resistance of cancer.American journal of cancer research · 2020Review
- The biogenesis and roles of extrachromosomal oncogene involved in carcinogenesis and evolution.American journal of cancer research · 2020Review
- Molecular characterization of cell-free eccDNAs in human plasma.Scientific reports · 2017Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
In primary brain tumors, oncogenes are frequently amplified and maintained on extrachromosomal DNA as double minutes (DM), but the underlying mechanisms remain poorly understood. We have generated a mouse model of malignant glioma based on knock-in of a mutant PDGF receptor α (PDGFRα) that is expressed in oligodendrocyte precursor cells (OPCs) after activation by a Cre recombinase. In the tumor suppressor INK4/Arf(-/-) background, mutant animals frequently developed brain tumors resembling anaplastic human gliomas (WHO grade III). Besides brain tumors, most animals also developed aggressive fibrosarcomas, likely triggered by Cre activation of mutant PDGFRα in fibroblastic cell lineages. Importantly, in the brain tumors and cell lines derived from brain tumor tissues, we identified a high prevalence of DM Pdgfra gene amplification, suggesting its occurrence as an early mutational event contributing to the malignant transformation of OPCs. Amplicons extended beyond the Pdgfra locus and included in some cases neighboring genes Kit and Kdr. Our genetically defined mouse brain tumor model therefore supports OPC as a cell of origin for malignant glioma and offers an example of a defined temporal sequence of mutational events, thus providing an entry point for a mechanistic understanding of DM gene amplification and its functionality in gliomagenesis.
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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.