ReviewNeuro-oncology2024
Cancer stem cell hypothesis 2.0 in glioblastoma: Where are we now and where are we going?
Review in Neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed.
- Development and characterization of triazole-based WDR5 inhibitors for the treatment of glioblastoma.JCI insight · 2026Article
- Computational design and immunoinformatics validation of a T cell multi-epitope vaccine targeting glioblastoma stem cells.Scientific reports · 2026Article
- Aptamer-functionalized exosomes combined with doxorubicin suppress GBM progression and enhance chemoradiosensitivity by promoting pyroptosis.Materials today. Bio · 2026Article
- Engineered exosomes for targeted glioma therapy: overcoming the blood-brain barrier with nature-inspired nanocarriers.Discover nano · 2026Review
- Oligodendrocyte transcription factor 2 orchestrates glioblastoma immune evasion by suppressing CXCL10 and CD8+ T cell activation.The Journal of clinical investigation · 2026Article
- EGFR/ZBED1 reciprocal regulation promotes stemness and tumorigenesis in glioblastoma.Neuro-oncology · 2026Article
- Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.Frontiers in oncology · 2026Review
- Cellular heterogeneity and therapeutic response profiling of human IDH + glioma stem cell cultures.Scientific reports · 2025Article
- The Role of Chaf1b in Maintaining Glioma Stem Cell Stemness and Regulating Microglial Polarization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Review
- RGS20 reduces glioma stemness and temozolomide resistance by intrinsically inhibiting the WNT/β-catenin signaling pathway.Scientific reports · 2025Article
- Histone Lactylation-Driven Upregulation of VRK1 Expression Promotes Stemness and Proliferation of Glioma Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Biology of stem cell paradox: a double-edged sword-implications for cancer therapy.Cancer cell international · 2025Review
- Exosomal non-coding RNAs: mediators of crosstalk between cancer and cancer stem cells.Cell death discovery · 2025Review
- Investigation of MANF regulation of glioma stemness via STAT3/TGF-β/SMAD4/p38 pathway based on pan-cancer analysis.Translational oncology · 2025Article
- Review
- A Murine Model of Glioblastoma Initiating Cells and Human Brain Organoid Xenograft for Photodynamic Therapy Testing.International journal of molecular sciences · 2025Article
- Towards non-invasive diagnosis of glioblastoma: identifying metabolic biomarkers in liquid biopsies using a ROC-based approach.Discover oncology · 2025Article
- Identification of the Oncogenic Role of MSH2 in the Stemness and Progression of Glioma Through Regulating Wnt Signaling Pathway.Cancer medicine · 2025Article
- Spatial epigenomic niches underlie glioblastoma cell state plasticity.bioRxiv : the preprint server for biology · 2025Article
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.
Funding
Abstract
Over the past 2 decades, the cancer stem cell (CSC) hypothesis has provided insight into many malignant tumors, including glioblastoma (GBM). Cancer stem cells have been identified in patient-derived tumors and in some mouse models, allowing for a deeper understanding of cellular and molecular mechanisms underlying GBM growth and therapeutic resistance. The CSC hypothesis has been the cornerstone of cellular heterogeneity, providing a conceptual and technical framework to explain this longstanding phenotype in GBM. This hypothesis has evolved to fit recent insights into how cellular plasticity drives tumor growth to suggest that CSCs do not represent a distinct population but rather a cellular state with substantial plasticity that can be achieved by non-CSCs under specific conditions. This has further been reinforced by advances in genomics, including single-cell approaches, that have used the CSC hypothesis to identify multiple putative CSC states with unique properties, including specific developmental and metabolic programs. In this review, we provide a historical perspective on the CSC hypothesis and its recent evolution, with a focus on key functional phenotypes, and provide an update on the definition for its use in future genomic studies.
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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.