ArticleGenes & development2020
Glioblastoma stem cells induce quiescence in surrounding neural stem cells via Notch signaling.
Article in Genes & development, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The subventricular zone structure, function and implications for neurological disease.Genes & diseases · 2025Review
- The Role of the Dysregulation of circRNAs Expression in Glioblastoma Multiforme.Journal of molecular neuroscience : MN · 2025Review
- Breaking the brain barrier: cell competition in neural development and disease.Neural regeneration research · 2024Article
- Cancer stem cell hypothesis 2.0 in glioblastoma: Where are we now and where are we going?Neuro-oncology · 2024Review
- Mutation of p53 increases the competitive ability of pluripotent stem cells.Development (Cambridge, England) · 2024Article
- Genetic Inactivation ofCancers · 2022Article
- Characterization of EGFR-reprogrammable temozolomide-resistant cells in a model of glioblastoma.Cell death discovery · 2022Article
- Opinion: Bridging gaps and doubts in glioblastoma cell-of-origin.Frontiers in oncology · 2022Article
- Old Stars and New Players in the Brain Tumor Microenvironment.Frontiers in cellular neuroscience · 2021Review
- Glioblastoma Proximity to the Lateral Ventricle Alters Neurogenic Cell Populations of the Subventricular Zone.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
There is increasing evidence demonstrating that adult neural stem cells (NSCs) are a cell of origin of glioblastoma. Here we analyzed the interaction between transformed and wild-type NSCs isolated from the adult mouse subventricular zone niche. We found that transformed NSCs are refractory to quiescence-inducing signals. Unexpectedly, we also demonstrated that these cells induce quiescence in surrounding wild-type NSCs in a cell-cell contact and Notch signaling-dependent manner. Our findings therefore suggest that oncogenic mutations are propagated in the stem cell niche not just through cell-intrinsic advantages, but also by outcompeting neighboring stem cells through repression of their proliferation.
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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.