Tumour angiogenesis, as distinguished from normal brain vasculature: molecular mechanisms & dependencies

How nutrients influence it

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What it does

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Recorded relationships

Where it participates (unsigned role)

In meningioma cell lines the half-maximal inhibitory concentration for mebendazole was 0.26 to 0.42 micromolar, mebendazole alone induced cytotoxicity but the combination with radiation gave a greater reduction in colony formation and higher levels of cleaved caspase-3, and in mice implanted intracranially with human meningioma both mebendazole alone and the combination gave a survival benefit with increased apoptosis and decreased tumour cell and vascular proliferation.
Mebendazole → Radiotherapy source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice
exposure
Mebendazole alone and combined with radiation
limitations
A combination study in one meningioma line and one implanted model. The mechanism is inferred from immunohistochemistry rather than dissected.
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 and mouse
plain_language
Added to radiation it killed more tumour cells than radiation alone.
primary_references
[mbz-p30414098] Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma. (2018). https://pubmed.ncbi.nlm.nih.gov/30414098/ DOI: 10.1007/s11060-018-03009-7
tissue_or_cell_type
Malignant meningioma
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 563–574
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice · source_derived_draft · unverified_draft
### mbz-adds-to-radiation In meningioma cell lines the half-maximal inhibitory concentration for mebendazole was 0.26 to 0.42 micromolar, mebendazole alone induced cytotoxicity but the combination with radiation gave a greater reduction in colony formation and higher levels of cleaved caspase-3, and in mice implanted intracranially with human meningioma both mebendazole alone and the combination gave a survival benefit with increased apoptosis and decreased tumour cell and vascular proliferation. 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: Added to radiation it killed more tumour cells than radiation alone. organism: Human cells and mouse tissue_or_cell_type: Malignant meningioma experimental_model: Colony formation, proliferation and caspase assays with intracranial human meningioma implants in mice limitations: A combination study in one meningioma line and one implanted model. The mechanism is inferred from immunohistochemistry rather than dissected. exposure: Mebendazole alone and combined with radiation evidence_span: {"source_cache": "artifacts/mebendazole-research/30414098.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400", "start_char": 0, "end_char": 1743, "text_sha256": "34445c01e56a2bfa33e4d1118f86c291fab041b15fa08da37592f4ec92d81400"} [mbz-p30414098] Mebendazole and radiation in combination increase survival through anticancer mechanisms in an intracranial rodent model of malignant meningioma. (2018). https://pubmed.ncbi.nlm.nih.gov/30414098/ DOI: 10.1007/s11060-018-03009-7
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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Situations it appears in

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In the sources

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Open hypotheses

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Tumour angiogenesis, as distinguished from normal brain vasculature