ArticleJournal of translational medicine2026
Single-cell multi-omic integration analysis prioritizes druggable genes and reveals cell-type-specific causal effects in glioblastomagenesis.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGliomas constitute 80% of malignant brain tumors, with glioblastoma (GBM) being the most aggressive subtype. The single-cell-level mechanisms underlying gliomagenesis are poorly understood, hindering therapeutic development. We combine genome-wide association studies (GWAS) with bulk tissue and single-cell multi-omics to prioritize genetically supported candidate genes and to explore potential cell-type-specific mechanisms relevant to gliomagenesis.
methodsWe integrated the largest glioma GWAS with brain-specific multi-omics to prioritize genetically supported candidate genes using two broad categories of prioritized methods. Biological enrichment, differential gene expression, and CRISPR/miRNA were used to assess target enrichment and druggability. By integrating single-cell multi-omics data (genomics, transcriptomics, epigenomics), we investigated GBM-relevant cells, tumor microenvironment (TME) interactions, and cell-type-specific mechanisms in glioblastomagenesis. Additionally, phenome-wide association studies (PheWAS) and drug repurposing analyses were conducted to annotate genetic pleiotropy and enhance drug repositioning.
resultsWe prioritized 11 high-confidence and 47 putatively causal genes, most of which are druggable. Astrocytes and oligodendrocyte precursor cells (OPCs) were implicated as GBM-relevant cell populations, with significantly increased TME cell communication between these populations and neurons. We further identified 14 putative cell-type-specific effects related to glioblastomagenesis, including three high-confidence genes (EGFR in astrocytes, CDKN2A in OPCs, and JAK1 in excitatory neurons). Most effects (85.7%, 12/14) were associated with non-GBM-relevant cell cells, encompassing both glial and neural cells.
conclusionsThis study systematically identifies genetically supported candidate genes in gliomagenesis and their cell-type-specific effects. These findings provide a resource for future mechanistic investigation and may help inform the development of more precise therapeutic hypotheses.
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