Fig. 6

Transcriptomic states of myeloid cells in human GBM. A UMAP projection of myeloid subsets from GBM patient tumors (103 patient tumors, GBmap datasets [39]). Cells are color coded for Mg and Mo ontogeny based on established gene signatures. Proportions of Mg and Mo are shown in individual GBM patient tumors. Recurrent tumors are marked with red asterisks. B Convergence of Mg and Mo to TAMs in GBM patient tumors. Heatmap showing overexpression scores (OES) of signatures in scRNA-seq primary (n = 7) and recurrent (n = 4) GBMs [8]. Each column represents a single cell. C Heatmap showing OES of signatures in different tumor locations from the IVY-GAP bulk RNA-seq data: LD edge: leading edge; Inf tumor: infiltrative tumor; HyBV: hyperplastic blood vessels in cellular tumor; MvP: microvascular proliferation. Each column represents a microdissected tissue fragment (n = 279 from 44 patient tumors). D Representative surface plots of the spatial localization of Mg and Mo signatures in GBM patient tumors. E Spatially weighted correlation analysis of the enrichment scores in myeloid transcriptomic states (CL0-8) linked to functional myeloid signatures, GBM tumor states, spatial TME niches, and TME cell components (n = 16 tumors from 16 individual patients). F Representative Iba1 stainings in GBM patient tumors. Cellular tumor and perinecrotic regions are shown for 2 patients. Red arrows depict Iba1⁺ myeloid cells with visible ramifications, Scale bar: 100 µm