ArticleCancer cell international2026
CD133 structural instability as a gateway to medulloblastoma vulnerability.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
backgroundMedulloblastoma (MB) is the most common malignant paediatric brain tumor. Among distinct MB subtypes, Group 3 represents one of the most aggressive subtypes, with high relapse rate, frequent metastasis, and mortality. These malignant traits are largely driven by MB stem cells (MBSCs), a subpopulation with enhanced self-renewal capacity and resistance to standard therapies, making them prime targets for innovative treatment strategies.
methodsGroup 3 MB human cell lines were treated with 0.3 µM Brefeldin A (BFA), a potent inducer of endoplasmic reticulum stress. Proteomic analyses via nano-LC-MS/MS were employed to investigate structural alterations in CD133, a key cell surface and stemness-associated receptor. Finally, computational screening was performed to identify Food and Drug Administration (FDA) and European Medicines Agency (EMA)-approved compounds, with improved pharmacokinetic and pharmacodynamic profiles that mimic BFA's mechanism of action.
resultsWe demonstrate that BFA induced structural disruption of CD133 and compromised MBSCs stem-like phenotype. This loss of stem-like properties correlates with diminished clonogenic potential, downregulation of the oncogenic PI3K/AKT/mTOR signaling axis, and impaired intercellular communication. Importantly, we identified clinically approved compounds capable of recapitulating the biological effects associated with BFA treatment.
conclusionsThis study uncovers a previously unrecognized mechanism of CD133 structural modulation and highlights the existence of clinically approved compounds that may impair MBSC function, offering a promising possible avenue for targeting therapy-resistant tumor-initiating cells in aggressive Group 3 MB.
Indexed as
Identifiers
What OpenQuestion holds
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.