ArticleCell reports2013
An aberrant transcription factor network essential for Wnt signaling and stem cell maintenance in glioblastoma.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
161 citing papers in PubMed, 1 synthesis or guideline pooled it, 279 citations in OpenAlex.
- Glioma Stem Cells as Promoter of Glioma Progression: A Systematic Review of Molecular Pathways and Targeted Therapies.International journal of molecular sciences · 2024Pooled it
- Integrating Molecular Pathology, Tumor Microenvironment, and Novel Therapies to Overcome Resistance in Glioblastoma.Journal of molecular neuroscience : MN · 2026Review
- ChromCall: assigning chromatin status to defined genomic regions using epigenomic profiling data.Bioinformatics (Oxford, England) · 2026Article
- A cellular epigenetic classification system for glioblastoma.Neuro-oncology · 2026Article
- SHH pathway inhibition and astrocyte co-culture induce distinct responses in glioblastoma and cancer stem cells.Scientific reports · 2026Article
- Review
- Targeting Wnt/β-catenin activation in combination with temozolomide leads to glioblastoma inhibition and long-term survival in mice.Genes & diseases · 2026Article
- A conserved differentiation programme facilitates inhibitory neuron production in the developing mouse and human cerebellum.Development (Cambridge, England) · 2025Article
- INSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model.Nature communications · 2025Article
- Wnt inhibition alleviates resistance to anti-PD1 therapy and improves antitumor immunity in glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Tumor heterogeneity and resistance in glioblastoma: the role of stem cells.Apoptosis : an international journal on programmed cell death · 2025Review
- Glioma stem cells: drivers of tumor progression and recurrence.Stem cell research & therapy · 2025Review
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
- The chemotherapy agent doxorubicin induces CNS expression of Ascl1, a regulator of adult neurogenesis and differentiation.Scientific reports · 2025Article
- Sonic hedgehog signalling pathway in CNS tumours: its role and therapeutic implications.Molecular brain · 2024Review
- HOXDeRNA activates a cancerous transcription program and super enhancers via genome-wide binding.Molecular cell · 2024Article
- Exosomal TNF-α mediates voltage-gated Na+ channel 1.6 overexpression and contributes to brain tumor-induced neuronal hyperexcitability.The Journal of clinical investigation · 2024Article
- Distinct Regulation of ASCL1 by the Cell Cycle and Chemotherapy in Small Cell Lung Cancer.Molecular cancer research : MCR · 2024Article
- Article
- IDHwt glioblastomas can be stratified by their transcriptional response to standard treatment, with implications for targeted therapy.Genome biology · 2024Article
101 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
14 authors at 5 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is thought to be driven by a subpopulation of cancer stem cells (CSCs) that self-renew and recapitulate tumor heterogeneity yet remain poorly understood. Here, we present a comparative analysis of chromatin state in GBM CSCs that reveals widespread activation of genes normally held in check by Polycomb repressors. These activated targets include a large set of developmental transcription factors (TFs) whose coordinated activation is unique to the CSCs. We demonstrate that a critical factor in the set, ASCL1, activates Wnt signaling by repressing the negative regulator DKK1. We show that ASCL1 is essential for the maintenance and in vivo tumorigenicity of GBM CSCs. Genome-wide binding profiles for ASCL1 and the Wnt effector LEF-1 provide mechanistic insight and suggest widespread interactions between the TF module and the signaling pathway. Our findings demonstrate regulatory connections among ASCL1, Wnt signaling, and collaborating TFs that are essential for the maintenance and tumorigenicity of GBM CSCs.
Indexed as
Identifiers
What OpenQuestion holds
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.