ReviewExperimental neurology2014
The role of stem cells and progenitors in the genesis of medulloblastoma.
Review in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Medulloblastoma stem cell programs: Molecular roadmaps of disease progression.Developmental cell · 2026Review
- Depletion of kinesin motor KIF20A to target cell fate control suppresses medulloblastoma tumour growth.Communications biology · 2021Article
- Downregulation of miR-326 and its host gene β-arrestin1 induces pro-survival activity of E2F1 and promotes medulloblastoma growth.Molecular oncology · 2021Article
- YBX1 Indirectly Targets Heterochromatin-Repressed Inflammatory Response-Related Apoptosis Genes through Regulating CBX5 mRNA.International journal of molecular sciences · 2020Article
- HDAC and MAPK/ERK Inhibitors Cooperate To Reduce Viability and Stemness in Medulloblastoma.Journal of molecular neuroscience : MN · 2020Article
- Histone Deacetylase Inhibitors in Pediatric Brain Cancers: Biological Activities and Therapeutic Potential.Frontiers in cell and developmental biology · 2020Review
- Transcriptional repressor REST drives lineage stage-specific chromatin compaction atScience signaling · 2019Article
- Recent advances in SHH medulloblastoma progression: tumor suppressor mechanisms and the tumor microenvironment.F1000Research · 2019Review
- The developmental origin of brain tumours: a cellular and molecular framework.Development (Cambridge, England) · 2018Review
- Estrogen and soy isoflavonoids decrease sensitivity of medulloblastoma and central nervous system primitive neuroectodermal tumor cells to chemotherapeutic cytotoxicity.BMC pharmacology & toxicology · 2017Article
- β-arrestin1-mediated acetylation of Gli1 regulates Hedgehog/Gli signaling and modulates self-renewal of SHH medulloblastoma cancer stem cells.BMC cancer · 2017Article
- MB3W1 is an orthotopic xenograft model for anaplastic medulloblastoma displaying cancer stem cell- and Group 3-properties.BMC cancer · 2016Article
- Functional Genomics Identifies Tis21-Dependent Mechanisms and Putative Cancer Drug Targets Underlying Medulloblastoma Shh-Type Development.Frontiers in pharmacology · 2016Article
- Cellular commitment in the developing cerebellum.Frontiers in cellular neuroscience · 2014Review
- The histone deacetylase inhibitor sodium butyrate promotes cell death and differentiation and reduces neurosphere formation in human medulloblastoma cells.Molecular neurobiology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer results from dysregulation of growth and survival pathways in normal stem cells and progenitors. Identifying the cells from which a tumor arises can facilitate the development of animal models and point to novel targets for therapy. Medulloblastoma is an aggressive tumor of the cerebellum that occurs predominantly in children. Recent genomic studies suggest that medulloblastoma consists of 4 major subgroups, each with distinct mutations and signaling pathway deregulations, and each potentially arising from distinct populations of stem cells and progenitors. Here we review the major types of progenitor cells in the cerebellum and discuss their role in the genesis of medulloblastoma.
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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.