ArticleCell reports2024
A simple and scalable zebrafish model of Sonic hedgehog medulloblastoma.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Decoding and Overcoming Temozolomide Resistance Through CRISPR/Cas Technologies.Molecular diagnosis & therapy · 2026Review
- Current Landscape of Preclinical Models for Pediatric Gliomas: Clinical Implications and Future Directions.Cancers · 2025Review
- EZH2 inhibitor and Vismodegib synergistically inhibit the growth and metastasis of medulloblastoma.Medical oncology (Northwood, London, England) · 2025Article
- Transforming growth factor-β-mediated regulation of atoh1-expressing neural progenitors is involved in the generation of cerebellar granule cells in larval and adult zebrafish.Development, growth & differentiation · 2025Article
- Development of an orthotopic medulloblastoma zebrafish model for rapid drug testing.Neuro-oncology · 2025Article
- Small Fish, Big Answers: Zebrafish and the Molecular Drivers of Metastasis.International journal of molecular sciences · 2025Review
- Medulloblastoma: biology and immunotherapy.Frontiers in immunology · 2025Review
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Abstract
Medulloblastoma (MB) is the most common malignant brain tumor in children and is stratified into three major subgroups. The Sonic hedgehog (SHH) subgroup represents ∼30% of all MB cases and has significant survival disparity depending upon TP53 status. Here, we describe a zebrafish model of SHH MB using CRISPR to create mutant ptch1, the primary genetic driver of human SHH MB. In these animals, tumors rapidly arise in the cerebellum and resemble human SHH MB by histology and comparative onco-genomics. Similar to human patients, MB tumors with loss of both ptch1 and tp53 have aggressive tumor histology and significantly worse survival outcomes. The simplicity and scalability of the ptch1-crispant MB model makes it highly amenable to CRISPR-based genome-editing screens to identify genes required for SHH MB tumor formation in vivo, and here we identify the gene encoding Grk3 kinase as one such target.
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