Figure 1.
Genetic and spatial determinants of myeloid heterogeneity. (A) Tumor mutations drive distinct myeloid phenotypic profiles across different tumors. (B) Myeloid cells can be compartmentalized within specific tumor regions (PDAC, NSCLC, breast cancer and brain metastasis are shown as examples), reflecting local microenvironmental cues. LOF, loss-of-function; OXPHOS, oxidative phosphorylation; SASP, senescence-associated secretory phenotype. The illustration is divided into two main sections. Section A, titled Mutational landscape as driver of myeloid cell heterogeneity, shows how various genetic mutations in different types of cancers influence the recruitment, phenotype, and functional diversity of myeloid cells. It includes diagrams of Lungs, Pancreas, Colon, Prostate, Brain (Metastasis), Breast, Ovaries/Uterus, and Liver cancers, highlighting specific mutations like Tp53, Kras, B R C A, Pten, and their associated myeloid cell markers and cytokines. Section B, titled Structural hubs of myeloid cells in the tumor microenvironment, depicts the spatial organization of myeloid cells within specific tumor regions, such as necrotic, perinecrotic, hypoxic, glycolytic, perivascular, and E M T areas, and their interactions with other cell types and the extracellular matrix. The legend identifies different cell types and their roles, such as neutrophils, macrophages, and tumor-associated macrophages.

Genetic and spatial determinants of myeloid heterogeneity. (A) Tumor mutations drive distinct myeloid phenotypic profiles across different tumors. (B) Myeloid cells can be compartmentalized within specific tumor regions (PDAC, NSCLC, breast cancer and brain metastasis are shown as examples), reflecting local microenvironmental cues. LOF, loss-of-function; OXPHOS, oxidative phosphorylation; SASP, senescence-associated secretory phenotype.

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