ArticleGenome biology2024
IDHwt glioblastomas can be stratified by their transcriptional response to standard treatment, with implications for targeted therapy.
Article in Genome biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Decoding and Overcoming Temozolomide Resistance Through CRISPR/Cas Technologies.Molecular diagnosis & therapy · 2026Review
- Hypoxia-induced circSPECC1 drives temozolomide resistance in glioblastoma via IGF2BP2-mediated PGK1 mRNA stabilization.Cell death & disease · 2026Article
- ChromCall: assigning chromatin status to defined genomic regions using epigenomic profiling data.Bioinformatics (Oxford, England) · 2026Article
- Review
- Spatial profiling of longitudinal glioblastoma reveals consistent changes in cellular architecture, post-treatment.Neuro-oncology · 2025Article
- Exploring Neural Stem Cell Therapies as Innovative Treatments for Glioblastoma.Cellular and molecular neurobiology · 2025Review
- Glioportal: a comprehensive transcriptomic resource unveiling ligand-mediated mesenchymal transition in glioblastoma.Neuro-oncology · 2025Article
- GBMPurity: A machine learning tool for estimating glioblastoma tumor purity from bulk RNA-sequencing data.Neuro-oncology · 2025Article
- Predictive modeling of glioblastoma recurrence for therapeutic target identification.EMBO molecular medicine · 2025Article
- The Complexity of Malignant Glioma Treatment.Cancers · 2025Review
- EZH2 functional dichotomy in reactive oxygen species-stratified glioblastoma.Neuro-oncology · 2025Article
- Concurrent RB1 and P53 pathway disruption predisposes to the development of a primitive neuronal component in high-grade gliomas depending on MYC-driven EBF3 transcription.Acta neuropathologica · 2025Article
- Longitudinal multimodal profiling of IDH-wildtype glioblastoma reveals the molecular evolution and cellular phenotypes underlying prognostically different treatment responses.Neuro-oncology · 2025Article
- Dual p38MAPK and MEK inhibition disrupts adaptive chemoresistance in mesenchymal glioblastoma to temozolomide.Neuro-oncology · 2024Article
- Identification of transcriptomic signatures associated with glioblastoma recurrence.Neuro-oncology · 2024Article
- IDHwt glioblastomas can be stratified by their transcriptional response to standard treatment, with implications for targeted therapy.Genome biology · 2024Article
- Molecular diversity in isocitrate dehydrogenase-wild-type glioblastoma.Brain communications · 2024Review
Corrections and comments
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Authors and funding
30 authors at 8 institutions in 2 countries.
Funding
Abstract
backgroundGlioblastoma (GBM) brain tumors lacking IDH1 mutations (IDHwt) have the worst prognosis of all brain neoplasms. Patients receive surgery and chemoradiotherapy but tumors almost always fatally recur.
resultsUsing RNA sequencing data from 107 pairs of pre- and post-standard treatment locally recurrent IDHwt GBM tumors, we identify two responder subtypes based on longitudinal changes in gene expression. In two thirds of patients, a specific subset of genes is upregulated from primary to recurrence (Up responders), and in one third, the same genes are downregulated (Down responders), specifically in neoplastic cells. Characterization of the responder subtypes indicates subtype-specific adaptive treatment resistance mechanisms that are associated with distinct changes in the tumor microenvironment. In Up responders, recurrent tumors are enriched in quiescent proneural GBM stem cells and differentiated neoplastic cells, with increased interaction with the surrounding normal brain and neurotransmitter signaling, whereas Down responders commonly undergo mesenchymal transition. ChIP-sequencing data from longitudinal GBM tumors suggests that the observed transcriptional reprogramming could be driven by Polycomb-based chromatin remodeling rather than DNA methylation.
conclusionsWe show that the responder subtype is cancer-cell intrinsic, recapitulated in in vitro GBM cell models, and influenced by the presence of the tumor microenvironment. Stratifying GBM tumors by responder subtype may lead to more effective treatment.
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