ArticleStem cells (Dayton, Ohio)2007
Cyclopamine-mediated hedgehog pathway inhibition depletes stem-like cancer cells in glioblastoma.
Article in Stem cells (Dayton, Ohio), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 300 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
300 citing papers in PubMed, 1 synthesis or guideline pooled it, 598 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
- Peptides from the Shadows: Molecular Depth Insights and Clinical Horizons of Circular RNA-encoded Peptides in Gliomas.Neuromolecular medicine · 2026Review
- Review
- SHH pathway inhibition and astrocyte co-culture induce distinct responses in glioblastoma and cancer stem cells.Scientific reports · 2026Article
- Small Molecule Cocktail DLC79 Suppresses Gliomagenesis by Activating Ascl1 and Remodeling Transcriptome.Cells · 2026Article
- Therapeutic potential of natural compounds in targeting cancer stem cells: a promising approach for cancer treatment.Discover oncology · 2025Review
- Natural Compounds That Target Glioma Stem Cells.NeuroSci · 2025Review
- Key roles of ubiquitination in regulating critical regulators of cancer stem cell functionality.Genes & diseases · 2025Review
- Review
- Resveratrol and temozolomide induce apoptosis and suppress proliferation in glioblastoma cells via the apoptotic signaling pathway.Acta cirurgica brasileira · 2025Article
- Brain microenvironment orchestrates highly aggressive tumor variants: current trends and therapeutic approaches.Frontiers in aging neuroscience · 2025Review
- Inorganic and hybrid nanomaterials for NIR-II fluorescence imaging-guided therapy of Glioblastoma and perspectives.Theranostics · 2025Review
- Practical immunomodulatory landscape of glioblastoma multiforme (GBM) therapy.Journal of the Egyptian National Cancer Institute · 2024Review
- Novel Anti-Cancer Stem Cell Compounds: A Comprehensive Review.Pharmaceutics · 2024Review
- Cancer stem cell hypothesis 2.0 in glioblastoma: Where are we now and where are we going?Neuro-oncology · 2024Review
- Emerging Therapies for Glioblastoma.Cancers · 2024Review
- Homeodomain Transcription Factors Nkx2.2 and Pax6 as Novel Biomarkers for Meningioma Tumor Treatment.Indian journal of clinical biochemistry : IJCB · 2024Article
- The intricate interplay between cancer stem cells and cell-of-origin of cancer: implications for therapeutic strategies.Frontiers in oncology · 2024Review
- Article
- Neural Stem Cells as Potential Glioblastoma Cells of Origin.Life (Basel, Switzerland) · 2023Review
240 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
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Brain tumors can arise following deregulation of signaling pathways normally activated during brain development and may derive from neural stem cells. Given the requirement for Hedgehog in non-neoplastic stem cells, we investigated whether Hedgehog blockade could target the stem-like population in glioblastoma multiforme (GBM). We found that Gli1, a key Hedgehog pathway target, was highly expressed in 5 of 19 primary GBM and in 4 of 7 GBM cell lines. Shh ligand was expressed in some primary tumors, and in GBM-derived neurospheres, suggesting a potential mechanism for pathway activation. Hedgehog pathway blockade by cyclopamine caused a 40%-60% reduction in growth of adherent glioma lines highly expressing Gli1 but not in those lacking evidence of pathway activity. When GBM-derived neurospheres were treated with cyclopamine and then dissociated and seeded in media lacking the inhibitor, no new neurospheres formed, suggesting that the clonogenic cancer stem cells had been depleted. Consistent with this hypothesis, the stem-like fraction in gliomas marked by both aldehyde dehydrogenase activity and Hoechst dye excretion (side population) was significantly reduced or eliminated by cyclopamine. In contrast, we found that radiation treatment of our GBM neurospheres increased the percentage of these stem-like cells, suggesting that this standard therapy preferentially targets better-differentiated neoplastic cells. Most importantly, viable GBM cells injected intracranially following Hedgehog blockade were no longer able to form tumors in athymic mice, indicating that a cancer stem cell population critical for ongoing growth had been removed. Disclosure of potential conflicts of interest is found at the end of this article.
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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.