ArticleNeuro-oncology2018
Divergent evolution of temozolomide resistance in glioblastoma stem cells is reflected in extracellular vesicles and coupled with radiosensitization.
Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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.
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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.
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Who cites it
100 citing papers in PubMed, 142 citations in OpenAlex.
- The Imbalance Between Tumor Immunosurveillance and Tumor Immune Escape in Glioblastoma.Immunology and cell biology · 2026Review
- The suppressor of cytokine signaling 3 regulates glioma stem cell maintenance and immune microenvironment through signal transducer and activator of transcription 3 signaling.Journal of cell communication and signaling · 2026Article
- Stanniocalcin 1 contributes to glioma stem cells phenotypic plasticity through NOTCH1/STAT3/GFPT2 axis.Oncogenesis · 2026Article
- Extracellular Vesicles in the Biology and Liquid Biopsy Diagnostics of Pediatric High-Grade Glioma - Emerging Findings and Opportunities.Journal of extracellular biology · 2026Review
- Targeting YRDC blocks codon-biased FABP7 translation and lipid droplet formation to overcome chemoresistance in glioblastoma.Oncogene · 2026Article
- Cryogenic Electron Microscopy of Extracellular Vesicles from Temozolomide-Treated Glioblastoma Cells Reveals Great Morphological Heterogeneity.Nanomaterials (Basel, Switzerland) · 2026Article
- Glioblastoma Cells Expressing Oncogenic EGFR Release Multiple Extracellular Vesicle Subpopulations Positive or Negative for EGFR.Journal of extracellular biology · 2026Article
- Review
- Engineered exosomes for targeted glioma therapy: overcoming the blood-brain barrier with nature-inspired nanocarriers.Discover nano · 2026Review
- Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis.Journal of advanced research · 2026Article
- Overcoming Intrinsic and Acquired Temozolomide Resistance in Glioblastoma: Fisetin as a Potential Strategy to Enhance Sensitivity via ZEB1 Modulation.Turkish journal of pharmaceutical sciences · 2026Article
- Atypical behavior of recurrent glioblastoma tumor cells with a highly adherent radial glial phenotype.CNS oncology · 2025Article
- LMNA-PRKDC axis enhances DNA repair and promotes chemoresistance in glioblastoma.Cell death & disease · 2025Article
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- Review
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Bypassing Blood-Brain Barrier and Glucose Dependency of Anti-Glioblastoma Drug Candidates Targeting Mitochondrial Respiration.Journal of cellular physiology · 2025Article
- Nanoparticle encapsulation enables systemic IGF-Trap delivery to inhibit intracerebral glioma growth.Neuro-oncology · 2025Article
- Targeting Glioblastoma Stem Cells: A40s Aptamer-NIR-Dye Conjugate for Glioblastoma Visualization and Treatment.Biomolecules · 2025Article
- Immune cell infiltration into brain tumor microenvironment is mediated by Rab27-regulated vascular wall integrity.Science advances · 2025Article
40 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
8 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioblastoma (GBM) is almost invariably fatal due to failure of standard therapy. The relapse of GBM following surgery, radiation, and systemic temozolomide (TMZ) is attributed to the ability of glioma stem cells (GSCs) to survive, evolve, and repopulate the tumor mass, events on which therapy exerts a poorly understood influence. Methods: Here we explore the molecular and cellular evolution of TMZ resistance as it emerges in vivo (xenograft models) in a series of human GSCs with either proneural (PN) or mesenchymal (MES) molecular characteristics. Results: We observed that the initial response of GSC-initiated intracranial xenografts to TMZ is eventually replaced by refractory growth pattern. Individual tumors derived from the same isogenic GSC line expressed divergent and complex profiles of TMZ resistance markers, with a minor representation of O6-methylguanine DNA methyltransferase (MGMT) upregulation. In several independent TMZ-resistant tumors originating from MES GSCs we observed a consistent diminution of mesenchymal features, which persisted in cell culture and correlated with increased expression of Nestin, decline in transglutaminase 2 and sensitivity to radiation. The corresponding mRNA expression profiles reflective of TMZ resistance and stem cell phenotype were recapitulated in the transcriptome of exosome-like extracellular vesicles (EVs) released by GSCs into the culture medium. Conclusions: Intrinsic changes in the tumor-initiating cell compartment may include loss of subtype characteristics and reciprocal alterations in sensitivity to chemo- and radiation therapy. These observations suggest that exploiting therapy-induced changes in the GSC phenotype and alternating cycles of therapy may be explored to improve GBM outcomes.
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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.