ArticleGenes & diseases2015
Glioblastoma stem cells (GSCs) epigenetic plasticity and interconversion between differentiated non-GSCs and GSCs.
Article in Genes & diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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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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Who cites it
145 citing papers in PubMed, 229 citations in OpenAlex.
- H2AX phosphorylation driven by the SET-PP2A axis maintains glioma stem cell properties.Genes & diseases · 2026Article
- Enhancer of Zeste Homolog 2 (EZH2): From Glioblastoma Biology to Potential Epigenetic Therapy.International journal of molecular sciences · 2026Review
- IQGAP3 bridges matrix stiffness with glioma stem cell maintenance and radioresistance by stabilizing SOX2.Nature communications · 2026Article
- C1orf226 Promotes Glioma Stemness and Oncogenesis in Glioma via PLK1-Mediated Wnt/β-Catenin Signaling.Cancer medicine · 2026Article
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- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- Clinical and genetic determinants of glioblastoma survival: a retrospective study.Frontiers in molecular neuroscience · 2026Article
- 3D Brain Vascular Niche Model Captures Glioblastoma Infiltration, Dormancy, and Gene Signatures.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cancer stem cells: Bridging microenvironmental interactions and clinical therapy.Clinical and translational medicine · 2025Review
- Rapidly progressive scalp and lung metastases with fatal pneumothorax in glioblastoma, IDH-wildtype, with MET and CDK6 amplifications: a case report of clinical course and postmortem autopsy, including genetic analysis.Brain tumor pathology · 2025Article
- Multi-Transcriptomic Analysis Reveals GSC-Driven MES-Like Differentiation via EMT in GBM Cell-Cell Communication.Biomedicines · 2025Article
- Temozolomide promotes glioblastoma stemness expression through senescence-associated reprogramming via HIF1α/HIF2α regulation.Cell death & disease · 2025Article
- Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies.International journal of molecular sciences · 2025Review
- Unravelling the link between circadian clock genes and brain tumors: From pathological disruptions to potential therapeutic interventions.Frontiers in pharmacology · 2025Review
- Endothelial cell-derived SDF-1α elicits stemness traits of glioblastomaTheranostics · 2025Article
- Nano-Encapsulated Taro Lectin Can Cross an in vitro Blood-Brain Barrier, Induce Apoptosis and Autophagy and Inhibit the Migration of Human U-87 MG Glioblastoma Cells.International journal of nanomedicine · 2025Article
- The epigenetic mechanisms involved in the treatment resistance of glioblastoma.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- MEG8 as an antagonistic pleiotropic mechanism in breast cancer.Cell death discovery · 2024Article
85 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
5 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer stem cells (CSCs) or cancer initiating cells (CICs) maintain self-renewal and multilineage differentiation properties of various tumors, as well as the cellular heterogeneity consisting of several subpopulations within tumors. CSCs display the malignant phenotype, self-renewal ability, altered genomic stability, specific epigenetic signature, and most of the time can be phenotyped by cell surface markers (e.g., CD133, CD24, and CD44). Numerous studies support the concept that non-stem cancer cells (non-CSCs) are sensitive to cancer therapy while CSCs are relatively resistant to treatment. In glioblastoma stem cells (GSCs), there is clonal heterogeneity at the genetic level with distinct tumorigenic potential, and defined GSC marker expression resulting from clonal evolution which is likely to influence disease progression and response to treatment. Another level of complexity in glioblastoma multiforme (GBM) tumors is the dynamic equilibrium between GSCs and differentiated non-GSCs, and the potential for non-GSCs to revert (dedifferentiate) to GSCs due to epigenetic alteration which confers phenotypic plasticity to the tumor cell population. Moreover, exposure of the differentiated GBM cells to therapeutic doses of temozolomide (TMZ) or ionizing radiation (IR) increases the GSC pool both
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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.