Evidence map›Paper›PMID 40664675›Full record

ArticleCell death & disease2025

Simvastatin suppresses spinal cord metastasis of medulloblastoma at clinically significant doses.

Charley Comer, Kian Cotton, Christopher Edwards, Xiaoyang Dai, Sara Badodi, Roberto Buccafusca, Chris Bennett, Andrew Peet, Alice Williams, David Michod and 2 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Charley ComerLife Science Department, University of Bath, Bath, UK.
Kian CottonLife Science Department, University of Bath, Bath, UK.ORCID http://orcid.org/0009-0008-5551-9412
Christopher EdwardsLife Science Department, University of Bath, Bath, UK.
Xiaoyang DaiBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Sara BadodiBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0002-8407-8336
Roberto BuccafuscaSchool of Physical and Chemical Sciences, Queen Mary University of London, London, UK.
Chris BennettInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Andrew PeetInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Alice WilliamsLife Science Department, University of Bath, Bath, UK.ORCID http://orcid.org/0009-0002-5664-9135
David MichodCancer Section, Development Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London, UK.ORCID http://orcid.org/0000-0002-4187-405X
Elena BochukovaBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Maria Victoria Niklison-ChirouBlizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. mvnc20@bath.ac.uk.ORCID http://orcid.org/0000-0002-2147-370X

Funding

Wellcome Trust
6 · The paper itself

Abstract

Medulloblastomas (MBs) are aggressive brain cancers and represent the most common primary malignant tumour in children. Current treatment protocols involve an intensive regimen of surgery, radiation therapy and chemotherapy, guided by histopathology and risk stratification. Unfortunately, disease relapse proves fatal in 30% of cases, and treatment efficacy is compromised as MB cells develop resistance. Therefore, there is a critical need for more effective and tolerable therapies, especially for the treatment of aggressive MBs associated with a poor prognosis. Lipid metabolism reprogramming, characterized by increased cholesterol synthesis, lipid uptake and the activation of de novo lipogenesis, is a newly identified hallmark of cancers. Cholesterol is an essential structural component of membranes that contributes to membrane integrity and fluidity. Recently, increasing evidence has indicated that cholesterol is a major determinant by modulating cell signalling events governing the hallmarks of cancer. Our research demonstrates there is an overexpression of cholesterol metabolism in group 3 (G3), and group 4 (G4) MB subgroups compared to Sonic Hedgehog (SHH)-MB subgroup. In these tumours, cholesterol metabolism supports cell migration through the Rho-GTPase signalling pathway. Notably, we observed that shifting the culture conditions from 2D to 3D significantly upregulates lipid metabolism. Furthermore, spheroids derived from G3/G4-MBs and SHH-MBs show similar sensitivity to low doses of simvastatin. We validated these findings in a xenograft mouse model, where treatment with low doses of simvastatin led to increased survival time and remarkably, also reduced the metastatic spread of MB cells to the spinal cord. These results suggest that simvastatin holds potential as an adjuvant treatment for patients with medulloblastoma.

Indexed as

Cerebellar NeoplasmsMedulloblastomaSimvastatinSpinal Cord NeoplasmsAnimalsCell Line, TumorCell MovementCholesterolHumansLipid MetabolismMiceSignal TransductionXenograft Model Antitumor AssaysCholesterolSimvastatin

Identifiers

PMID40664675
PMCPMC12263873

What OpenQuestion holds

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Registered trials

None linked

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.