Growth of medulloblastoma cells and allografts: molecular mechanisms & dependencies

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What it does

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Recorded relationships

Where it participates (unsigned role)

Mebendazole potently inhibited hedgehog signalling and slowed the growth of hedgehog-driven human medulloblastoma cells at clinically attainable concentrations, suppressed formation of the primary cilium, a microtubule-based organelle that functions as a signalling hub for pathway activation, and its inhibition was unaffected by mutants in the gene encoding human Smoothened that are selectively propagated in clones surviving vismodegib, with the combination of vismodegib and mebendazole giving additive inhibition.
Mebendazole → Hedgehog signalling source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Hedgehog reporter and medulloblastoma cell growth assays with Smoothened mutant lines
exposure
Mebendazole at clinically attainable concentrations, alone and with vismodegib
limitations
Proposes a second mechanism which is still microtubule-based, through the primary cilium. Cell assays; the claim that the concentrations are clinically attainable is the authors’.
nutrient_topic
Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole
organism
Human cells
plain_language
It blocks this growth pathway by removing the little antenna the pathway needs, so mutations that defeat the standard drug do not defeat it.
primary_references
[mbz-p25376612] Repurposing the antihelmintic mebendazole as a hedgehog inhibitor. (2015). https://pubmed.ncbi.nlm.nih.gov/25376612/ DOI: 10.1158/1535-7163.mct-14-0755-t
tissue_or_cell_type
Medulloblastoma
Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 537–548
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hedgehog reporter and medulloblastoma cell growth assays with Smoothened mutant lines · source_derived_draft · unverified_draft
### mbz-hedgehog-through-the-cilium Mebendazole potently inhibited hedgehog signalling and slowed the growth of hedgehog-driven human medulloblastoma cells at clinically attainable concentrations, suppressed formation of the primary cilium, a microtubule-based organelle that functions as a signalling hub for pathway activation, and its inhibition was unaffected by mutants in the gene encoding human Smoothened that are selectively propagated in clones surviving vismodegib, with the combination of vismodegib and mebendazole giving additive inhibition. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: It blocks this growth pathway by removing the little antenna the pathway needs, so mutations that defeat the standard drug do not defeat it. organism: Human cells tissue_or_cell_type: Medulloblastoma experimental_model: Hedgehog reporter and medulloblastoma cell growth assays with Smoothened mutant lines limitations: Proposes a second mechanism which is still microtubule-based, through the primary cilium. Cell assays; the claim that the concentrations are clinically attainable is the authors’. exposure: Mebendazole at clinically attainable concentrations, alone and with vismodegib evidence_span: {"source_cache": "artifacts/mebendazole-research/25376612.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa6b6f06dfda62c5f1cc59df64f813c5d112f8d6a3bf969c6fa4432073a87ec0", "start_char": 0, "end_char": 1290, "text_sha256": "fa6b6f06dfda62c5f1cc59df64f813c5d112f8d6a3bf969c6fa4432073a87ec0"} [mbz-p25376612] Repurposing the antihelmintic mebendazole as a hedgehog inhibitor. (2015). https://pubmed.ncbi.nlm.nih.gov/25376612/ DOI: 10.1158/1535-7163.mct-14-0755-t
Complete structured claim and evidence
Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib.
Mebendazole → Vascular endothelial growth factor receptor 2 / KDR source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"}
experimental_model
Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models
exposure
Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model
limitations
Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here.
nutrient_topic
Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole
organism
Mouse
plain_language
It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones.
primary_references
[mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234
tissue_or_cell_type
Medulloblastoma and tumour vasculature
Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 550–561
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models · source_derived_draft · unverified_draft
### mbz-vegfr2-atp-competition Mebendazole was determined to interfere with vascular endothelial growth factor receptor 2 kinase by competing with ATP, selectively inhibited tumour angiogenesis but not the normal brain vasculature in orthotopic medulloblastoma models, suppressed the kinase in vivo, and significantly extended survival of medulloblastoma models derived from different molecular backgrounds including a PTCH1-mutant tumour with acquired resistance to the smoothened inhibitor vismodegib. Condition category: normal nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: It also blocks the receptor that grows new tumour blood vessels, and spares the normal ones. organism: Mouse tissue_or_cell_type: Medulloblastoma and tumour vasculature experimental_model: Autophosphorylation and cell-free kinase assays with orthotopic medulloblastoma allograft and xenograft models limitations: Identifies a third mechanism, kinase inhibition, with a defined competition mode. Whether this operates at achievable human concentrations is not established here. exposure: Mebendazole in PTCH1-mutant allografts, a group 3 xenograft and a vismodegib-resistant model evidence_span: {"source_cache": "artifacts/mebendazole-research/25253417.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169", "start_char": 0, "end_char": 1798, "text_sha256": "96333adbb3bce735b14f3c51317229543279992c3cd170760cc494566e49a169"} [mbz-p25253417] Effective treatment of diverse medulloblastoma models with mebendazole and its impact on tumor angiogenesis. (2015). https://pubmed.ncbi.nlm.nih.gov/25253417/ DOI: 10.1093/neuonc/nou234
Complete structured claim and evidence

The events it takes part in

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Open hypotheses

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Growth of medulloblastoma cells and allografts