ArticleNature communications2019
Stem cell-associated heterogeneity in Glioblastoma results from intrinsic tumor plasticity shaped by the microenvironment.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06492486 (Glioma Adaptive Radiotherapy With Development of an Artificial Intelligence Workflow), which is not on this map. Cited by 347 papers, 1 of them a synthesis that pooled it.
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.
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.
Glioma Adaptive Radiotherapy With Development of an Artificial Intelligence Workflow
Who cites it
347 citing papers in PubMed, 1 synthesis or guideline pooled it, 535 citations in OpenAlex.
- Unlocking glioblastoma: breakthroughs in molecular mechanisms and next-generation therapies.Medical oncology (Northwood, London, England) · 2025Pooled it
- Cancer stem cell assay-guided chemotherapy improves survival of patients with recurrent glioblastoma in a randomized trial.Cell reports. Medicine · 2023Trial
- CDState Resolves Malignant Cell Heterogeneity from Bulk Tumor RNA Sequencing Data.Cancer research · 2026Article
- Heterogeneity in cancer: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- RNA modifications as determinants of cancer cell death: from epitranscriptomic mechanisms to therapeutic targeting.Functional & integrative genomics · 2026Review
- Improving T-cell engager efficacy in glioblastoma with multi-antigen targeting and novel delivery approaches.Acta neuropathologica · 2026Review
- Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Hypoxic CA9-high mesenchymal-like glioma stem cells promote ANXA1-FPR1-dependent macrophage polarization in recurrent glioblastoma.Journal of neuroinflammation · 2026Article
- Decoding glioblastoma evolution and heterogeneity through mechanistic modeling: implications for clinical translation.Journal of experimental & clinical cancer research : CR · 2026Review
- Article
- Peptides from the Shadows: Molecular Depth Insights and Clinical Horizons of Circular RNA-encoded Peptides in Gliomas.Neuromolecular medicine · 2026Review
- High mannose content of mesenchymal glioblastoma correlates with hydroxyl proton transfer-weighted (HPTw) MRI as noninvasive biomarker of tumor aggressiveness.Science advances · 2026Article
- Article
- Cellular and inflammatory characteristics of patient‑derived glioblastoma organoids duringOncology reports · 2026Article
- Review
- Inhibition of cell surface GRP78 on brain tumors reverses drug resistance and stops cancer stem cell expansion.The Journal of biological chemistry · 2026Article
- Review
- Glioblastoma cells that evade chemoradiotherapy-induced cell death exhibit a bifurcated glycolytic program.Cell death & disease · 2026Article
- Review
- Effective approaches in conquering chemoresistance of glioblastoma: potential for nanoformulations.Drug delivery and translational research · 2026Review
287 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
22 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The identity and unique capacity of cancer stem cells (CSC) to drive tumor growth and resistance have been challenged in brain tumors. Here we report that cells expressing CSC-associated cell membrane markers in Glioblastoma (GBM) do not represent a clonal entity defined by distinct functional properties and transcriptomic profiles, but rather a plastic state that most cancer cells can adopt. We show that phenotypic heterogeneity arises from non-hierarchical, reversible state transitions, instructed by the microenvironment and is predictable by mathematical modeling. Although functional stem cell properties were similar in vitro, accelerated reconstitution of heterogeneity provides a growth advantage in vivo, suggesting that tumorigenic potential is linked to intrinsic plasticity rather than CSC multipotency. The capacity of any given cancer cell to reconstitute tumor heterogeneity cautions against therapies targeting CSC-associated membrane epitopes. Instead inherent cancer cell plasticity emerges as a novel relevant target for treatment.
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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.