ArticleProceedings of the National Academy of Sciences of the United States of America2014
In vivo radiation response of proneural glioma characterized by protective p53 transcriptional program and proneural-mesenchymal shift.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 182 citations in OpenAlex.
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- Monitoring glioblastoma extracellular vesicle evolution using a nanodiagnostic platform to detect glioma stem cells driving recurrent disease.Science advances · 2026Article
- C/EBPβ-induced alternative splicing of RCAN1 generates a potent TCR-T target in mesenchymal glioblastoma.Cellular & molecular immunology · 2026Article
- It's all downstream from here: RTK/Raf/MEK/ERK pathway resistance mechanisms in glioblastoma.Journal of neuro-oncology · 2025Review
- Exploring the regulatory role of CNPY3 as a prognostic biomarker on human glioma cell migration, invasion and immune infiltration.Cancer biomarkers : section A of Disease markers · 2025Article
- Network analyses of brain tumor multiomic data reveal pharmacological opportunities to alter cell state transitions.NPJ systems biology and applications · 2025Article
- Mesenchymal Properties of Glioma Cell Lines.Bulletin of experimental biology and medicine · 2024Article
- Glioblastoma microenvironment-from biology to therapy.Genes & development · 2024Review
- Gene regulatory network topology governs resistance and treatment escape in glioma stem-like cells.Science advances · 2024Article
- Review
- Multiplexed single-cell lineage tracing of mitotic kinesin inhibitor resistance in glioblastoma.Cell reports · 2024Article
- Network Analyses of Brain Tumor Patients' Multiomic Data Reveals Pharmacological Opportunities to Alter Cell State Transitions.Research square · 2024Article
- Network Analyses of Brain Tumor Patients' Multiomic Data Reveals Pharmacological Opportunities to Alter Cell State Transitions.bioRxiv : the preprint server for biology · 2024Article
- Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition.Cancer biology & medicine · 2024Review
- miRNA-194-3p represses NF-κB in gliomas to attenuate iPSC genes and proneural to mesenchymal transition.iScience · 2024Article
- CRISPR-Cas9 library screening combined with an exosome-targeted delivery system addresses tumorigenesis/TMZ resistance in the mesenchymal subtype of glioblastoma.Theranostics · 2024Article
- Understanding Glioblastoma Signaling, Heterogeneity, Invasiveness, and Drug Delivery Barriers.International journal of molecular sciences · 2023Review
- Multiplexed single-cell lineage tracing of mitotic kinesin inhibitor resistance in glioblastoma.bioRxiv : the preprint server for biology · 2023Article
- Tissue factor is a critical regulator of radiation therapy-induced glioblastoma remodeling.Cancer cell · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Glioblastoma is the most common adult primary brain tumor and has a dismal median survival. Radiation is a mainstay of treatment and significantly improves survival, yet recurrence is nearly inevitable. Better understanding the radiation response of glioblastoma will help improve strategies to treat this devastating disease. Here, we present a comprehensive study of the in vivo radiation response of glioma cells in a mouse model of proneural glioblastoma. These tumors are a heterogeneous mix of cell types with differing radiation sensitivities. To explicitly study the gene expression changes comprising the radiation response of the Olig2(+) tumor bulk cells, we used translating ribosome affinity purification (TRAP) from Olig2-TRAP transgenic mice. Comparing both ribosome-associated and total pools of mRNA isolated from Olig2(+) cells indicated that the in vivo gene expression response to radiation occurs primarily at the total transcript level. Genes related to apoptosis and cell growth were significantly altered. p53 and E2F were implicated as major regulators of the radiation response, with p53 activity needed for the largest gene expression changes after radiation. Additionally, radiation induced a marked shift away from a proneural expression pattern toward a mesenchymal one. This shift occurs in Olig2(+) cells within hours and in multiple genetic backgrounds. Targets for Stat3 and CEBPB, which have been suggested to be master regulators of a mesenchymal shift, were also up-regulated by radiation. These data provide a systematic description of the events following radiation and may be of use in identifying biological processes that promote glioma radioresistance.
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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.