Fig. 1: H3.3K27M drives tumorigenesis with genomic changes consistent with DIPG.
From: Epigenetic activation of a RAS/MYC axis in H3.3K27M-driven cancer
a Survival plot (all-cause mortality) of H3.3K27M mice (red line, n = 36) versus CD1 control mice (blue line, n = 662)27. Significance was determined at 24 months. b Pie charts showing the percentage deaths of H3.3K27M and CD1 mice (top, CD1 data from28,29,30) arising from cancer (black) or other causes (grey). The frequency of different tumour types amongst the cancer-related deaths are shown in the coloured pie charts for each genotype where red=carcinoma, blue=lymphoma, purple=osteosarcoma, green=other sarcoma and orange=high grade glioma (HGG) (bottom). c Haematoxylin and Eosin (H&E) staining of representative tumours from H3.3K27M mice. Scale bar: 100 µm. d Kaplan-Meier survival analysis of H3.3K27M, H3.3K27M/Trp53+/−, H3.3K27M/Trp53−/− and Trp53−/− mice31. e Somatic mutation burden (single-nucleotide variants/indels per megabase (MB) of exome) of human DIPG (n = 41), mouse HGG (n = 2), and human (n = 5) and mouse (n = 8) non-gliomas. Mouse tumours are coloured by type as in h. f Comparison of the fraction of the genome altered between human DIPG (n = 41) and mouse (n = 10) tumours. Mouse tumours are coloured by type as in h. g Comparison of copy number alteration (CNA) burden between human DIPG (n = 41) and mouse (n = 10). Mouse tumours are coloured by type as in h. h Oncoprint of tumour type, H3.3K27M and Trp53 genotype plus specific SNVs and focal CNAs. Source data are provided as a Source Data file. Statistical tests: Yates’ Chi-squared (a), log rank (d), t (e, f, g). NS: Not significant.
