ArticleCell death and differentiation2014
Conversion of differentiated cancer cells into cancer stem-like cells in a glioblastoma model after primary chemotherapy.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 1 of them a synthesis that pooled it.
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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
219 citing papers in PubMed, 1 synthesis or guideline pooled it, 336 citations in OpenAlex.
- A Systematic Review of the Metabolism of High-Grade Gliomas: Current Targeted Therapies and Future Perspectives.International journal of molecular sciences · 2024Pooled it
- Review
- EIF3B is associated with mBMC cancer · 2026Article
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Stress granules restrain ferroptosis by sequestering ferritin.Nature cell biology · 2026Article
- Review
- Mitochondrial DNA Content Modulates Chemosensitivity and Cellular Adaptation in Glioblastoma Cells.The Eurasian journal of medicine · 2026Article
- Dual suppression of stemness and redox adaptation in glioblastoma through filaggrin upregulation by an abiraterone-based HDAC inhibitor.Journal of biomedical science · 2026Article
- Metabolic dependencies and neural progenitor dysregulation: driving forces in paediatric high-grade glioma development.Cancer metastasis reviews · 2026Review
- Spatial heterogeneity of malignant molecular markers in glioma revealed by stereotactic biopsy.Discover oncology · 2026Article
- Review
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- The evolution of chemotherapy in brain tumors: from historical milestones to precision medicine in glioblastoma.Exploration of targeted anti-tumor therapy · 2026Review
- Invasive properties of patient-derived glioblastoma cells after reversible electroporationRadiology and oncology · 2025Article
- Par6/SOX2 interact to modulate stemness maintenance in glioma by regulating the EGFR/PI3K/AKT signaling cascade.Oncogene · 2025Article
- Plant-derived extracellular vesicles as a natural drug delivery platform for glioblastoma therapy: A dual role in preserving endothelial integrity while modulating the tumor microenvironment.International journal of pharmaceutics: X · 2025Article
- LMNA-PRKDC axis enhances DNA repair and promotes chemoresistance in glioblastoma.Cell death & disease · 2025Article
- Spatial self-organization of cancer stem cell niches revealed by live single-cell imaging.Stem cell research & therapy · 2025Article
- Machine learning on multiple epigenetic features reveals H3K27Ac as a driver of gene expression prediction across patients with glioblastoma.PLoS computational biology · 2025Article
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
159 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 1 institution in 1 country.
Funding
Abstract
Glioblastoma multiforme patients have a poor prognosis due to therapeutic resistance and tumor relapse. It has been suggested that gliomas are driven by a rare subset of tumor cells known as glioma stem cells (GSCs). This hypothesis states that only a few GSCs are able to divide, differentiate, and initiate a new tumor. It has also been shown that this subpopulation is more resistant to conventional therapies than its differentiated counterpart. In order to understand glioma recurrence post therapy, we investigated the behavior of GSCs after primary chemotherapy. We first show that exposure of patient-derived as well as established glioma cell lines to therapeutic doses of temozolomide (TMZ), the most commonly used antiglioma chemotherapy, consistently increases the GSC pool over time both in vitro and in vivo. Secondly, lineage-tracing analysis of the expanded GSC pool suggests that such amplification is a result of a phenotypic shift in the non-GSC population to a GSC-like state in the presence of TMZ. The newly converted GSC population expresses markers associated with pluripotency and stemness, such as CD133, SOX2, Oct4, and Nestin. Furthermore, we show that intracranial implantation of the newly converted GSCs in nude mice results in a more efficient grafting and invasive phenotype. Taken together, these findings provide the first evidence that glioma cells exposed to chemotherapeutic agents are able to interconvert between non-GSCs and GSCs, thereby replenishing the original tumor population, leading to a more infiltrative phenotype and enhanced chemoresistance. This may represent a potential mechanism for therapeutic relapse.
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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.