ArticleFrontiers in immunology2026
A transcriptome-defined TAM-rich phenotype identifies a macrophage-enriched, hypoxia-linked immune contexture in glioblastoma: multi-cohort transcriptomic validation and local histopathological correlation.
Article in Frontiers in immunology, 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
Background: Tumor-associated macrophages (TAMs) are a major immune component of the glioblastoma microenvironment, but macrophage-oriented transcriptomic stratification remains difficult to reproduce across datasets and to validate at the tissue level. Methods: TCGA-GBM was used as the discovery cohort, and two independent CGGA cohorts (CGGA_693 and CGGA_325) were used for external validation. A continuous transcriptome-defined TAM score was constructed Results: In TCGA, the TAM-rich phenotype was associated with broad upregulation of macrophage- and myeloid-related genes. Across TCGA, CGGA_693, and CGGA_325, macrophage-associated markers, including CD163, MSR1, MRC1, CSF1R, SPP1, VSIG4, MARCO, and TREM1, were consistently increased, and the hypoxia-associated marker CA9 was also elevated. By contrast, CD8A, CXCL9, and CXCL10 showed only modest concordant increases. External immune benchmark analyses using xCell macrophage-related scores and published no-TAM5 macrophage/TAM signatures supported concordance with macrophage-related immune context, and random-panel and label-permutation analyses reduced concern that the associations reflected arbitrary five-gene scoring or random grouping. Survival association was modest and cohort-dependent. In the local cohort, CD163-defined macrophage-enriched tumors showed higher CD163-positive and CD68-positive macrophage density, greater CAIX-positive area, and a lower CD8/CD163 ratio, reflecting relative macrophage dominance rather than absolute loss of CD8-positive cells. Conclusions: A compact transcriptome-defined TAM-rich phenotype captures a biologically reproducible, macrophage-enriched and hypoxia-linked immune contexture in glioblastoma. It should be interpreted primarily as a quantitative immune-state classifier and tissue-correlated biological stratifier, rather than as a uniformly independent prognostic factor.
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