ArticleNature neuroscience2025
Brain tumors induce widespread disruption of calvarial bone and alteration of skull marrow immune landscape.
Article in Nature neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Article
- Article
- Combined Molecular Hydrogen and Vitamin C Treatment in Irradiated Normal and Cancer Cell Models: An Exploratory In Vitro Study and Case Reports.Medical sciences (Basel, Switzerland) · 2026Article
- Spatially Distinct Bone Marrow Sites Are Asymmetrically Impacted by Inflammatory Cardiovascular Disease.JACC. Basic to translational science · 2026Article
- Depletion of CARM1 slows in vivo tumorigenicity and rewires developmental programming in glioma stem-like cells.Cell reports · 2026Article
- An irradiation-free platform for localized skull bone marrow manipulation to dissect the skull-brain axis.Journal of neuroinflammation · 2026Article
- Antigen-specific CD8 T cells are generated and reactivated in the bone marrow following viral brain infections and impact the bone marrow niche.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
28 authors.
Funding
Abstract
The skull marrow niche has recently been identified as a reservoir that supplies the brain with monocytes and neutrophils in the context of disease and injury, but its role in brain cancers remains unknown. Here we show that glioblastoma, the most malignant type of brain tumor, induces calvarial bone abnormalities in murine models and patients with glioblastoma, altering osteoclast activities and increasing the number of skull channels in mice. Single-cell RNA sequencing revealed glioblastoma-mediated alterations in the immune landscape of skull marrow and femoral bone marrow, including expansion of neutrophils and deterioration of various B cell subsets. In vivo inhibition of bone resorption reduced bone abnormalities, but promoted tumor progression in mesenchymal subtype tumors. This also abolished the survival benefit of the checkpoint inhibitor anti-PD-L1, by reducing activated T cell and increasing inflammatory neutrophil numbers. Together, these data provide insight into how brain tumors affect skull bone and the immune environment.
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