GSE160669
mRNASeq of glioma cells
In mouse models of PDGF-driven glioma where Notch is tumor-suppressive, we find that Notch activity shapes interferon-response in tumor cells and the local immune microenvironment early during tumor progression. Notch inhibition disturbs cytokine expression by tumor cells, altering recruitment and activation of immune cell populations and favoring hyper-proliferative "immune niche" independent growth. Genetic inactivation of Notch in glioma cells also attenuates their response to interferon-gamma, establishing a non-cell autonomous inhibitory feedback loop that further promotes immune evasion and aggressiveness. Hence, we propose that Notch signaling levels in tumor cells are key to orchestrate immune escape and microenvironment independency during brain tumor formation. Overall design: Expression profiles of PDGF+Trp53-/- glioma cells from tumors with four different Notch mutant genotypes (Rbpj-/-, Notch1-/-Notch2-/-, Notch1-/-, and Notch2-/-) and tumors with intact Notch signaling (PDGF+Trp53-/- control tumors)