PDGF signaling cooperates with H3.3K27M to increase tumor malignancy from Histone H3.3K27M Represses p16 to Accelerate Gliomagenesis in a Murine Model of DIPG

A. Analysis of tumor volume of PDGF driven, p53 WT models with expression of H3.3K27M (n= 6), H3.3WT (n= 6), or empty vector (n= 7) shows trend for larger tumors with mutation compared to H3.3WT (p= 0.25) or empty vector (p= 0.28) controls. B. Kaplan-Meier survival curve of murine tumors driven by co-injection of nestin tv-a; p53 floxed mice with RCAS-PDGFB; RCAS-Cre; and either RCAS-H3.3K27M-GFP (n=12) or RCAS-H3.3WT-GFP (n= 18). C. In vivo proliferation quantification of H3.3K27M or H3.3WT expressing tumors driven by PDGFB overexpression and p53 knockout using pH3 (H3.3K27M n= 5, H3.3WT n=4) or D. EdU incorporation IF quantification (n=3 each) E. Histone extraction followed by western blot using total H3 antibody comparing murine tumor cells infected with empty vector, H3.3WT, or H3.3K27M to determine the amount of H3 overexpression.