ArticleActa neuropathologica communications2023
Decoding key cell sub-populations and molecular alterations in glioblastoma at recurrence by single-cell analysis.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- EDNRB-dependent endothelin signaling reduces proliferation and promotes proneural-to-mesenchymal transition in gliomas.Molecular oncology · 2026Article
- Unraveling lncRNA diversity at a single cell resolution and in a spatial context across different cancer types.Nature methods · 2026Article
- Tumor microenvironment shapes the spatial organization of glioblastoma cell states.Neuro-oncology · 2026Review
- Extracellular matrix stiffness conditions glioblastoma cells for long-term migration: Mechanical memory as a driver of invasion and recurrence in glioblastoma.Neuro-oncology · 2026Review
- Integrated Multi-Omics Profiling Identifies CD84-Associated Microglial Alterations in Focal Cortical Dysplasia Type II.Journal of inflammation research · 2026Article
- PLX3397 attenuated tumor growth and remodeled tumor microenvironment of recurrent glioblastoma.Scientific reports · 2025Article
- Atypical behavior of recurrent glioblastoma tumor cells with a highly adherent radial glial phenotype.CNS oncology · 2025Article
- Investigating the impact of MCTP2 on immune suppression and drug resistance in glioblastoma.Functional & integrative genomics · 2025Article
- Contribution of Prostaglandin E2-Induced Neuronal Excitation to Drug Resistance in Glioblastoma Countered by a Novel Blood-Brain Barrier Crossing Celecoxib Derivative.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MOADE: a multimodal autoencoder for dissociating bulk multi-omics data.Genome biology · 2025Article
- Precision Neuro-Oncology in Glioblastoma: AI-Guided CRISPR Editing and Real-Time Multi-Omics for Genomic Brain Surgery.International journal of molecular sciences · 2025Review
- Multiplexed phosphoproteomics of low cell numbers using SPARCE.Communications biology · 2025Article
- Current landscape and future directions of targeted-alpha-therapy for glioblastoma treatment.Theranostics · 2025Review
- LAT4 drives temozolomide induced radiotherapy resistance in glioblastoma by enhancing mTOR pathway activation.Cancer cell international · 2024Article
- Single-cell multi-omics sequencing uncovers region-specific plasticity of glioblastoma for complementary therapeutic targeting.Science advances · 2024Article
- Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most frequent malignant brain tumor, the relapse of which is unavoidable following standard treatment. However, the effective treatment for recurrent GBM is lacking, necessitating the understanding of key mechanisms driving tumor recurrence and the identification of new targets for intervention. Here, we integrated single-cell RNA-sequencing data spanning 36 patient-matched primary and recurrent GBM (pGBM and rGBM) specimens, with 6 longitudinal GBM spatial transcriptomics to explore molecular alterations at recurrence, with each cell type characterized in parallel. Genes involved in extracellular matrix (ECM) organization are preferentially enriched in rGBM cells, and MAFK is highlighted as a potential regulator. Notably, we uncover a unique subpopulation of GBM cells that is much less detected in pGBM and highly expresses ECM and mesenchyme related genes, suggesting it may contribute to the molecular transition of rGBM. Further regulatory network analysis reveals that transcription factors, such as NFATC4 and activator protein 1 members, may function as hub regulators. All non-tumor cells alter their specific sets of genes as well and certain subgroups of myeloid cells appear to be physically associated with the mesenchyme-like GBM subpopulation. Altogether, our study provides new insights into the molecular understanding of GBM relapse and candidate targets for rGBM treatment.
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