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Glioblastoma (GBM) recurrence originates from invasive margin cells that escape surgical debulking, but to what extent these cells resemble their bulk counterparts remains unclear. Here, we generated three immunocompetent somatic GBM mouse models, driven by subtype-associated mutations, to compare matched bulk and margin cells. We find that, regardless of mutations, tumors converge on common sets of neural-like cellular states. However, bulk and margin have distinct biology. Injury-like programs associated with immune infiltration dominate in the bulk, leading to the generation of lowly proliferative injured neural progenitor-like cells (iNPCs). iNPCs account for a significant proportion of dormant GBM cells and are induced by interferon signaling within T cell niches. In contrast, developmental-like trajectories are favored within the immune-cold margin microenvironment resulting in differentiation toward invasive astrocyte-like cells. These findings suggest that the regional tumor microenvironment dominantly controls GBM cell fate and biological vulnerabilities identified in the bulk may not extend to the margin residuum. [Display omitted] • Somatic GBM mouse models were developed to compare tumor bulk and margin biology • GBM cell fates are imposed by tumor region independent of driver mutations • T cell-induced dormancy prevails in bulk, astrocyte-like differentiation in margin • Bulk and margin cells are functionally distinct subpopulations Garcia-Diaz et al. develop immunocompetent and disease-relevant somatic mouse models of glioblastoma to reveal that tumor bulk and margin cells have distinct biology, including differences in dormancy, differentiation trajectories, immune recruitment, and invasive and tumorigenic potential. [ABSTRACT FROM AUTHOR]