Fig. 1: PI3K-AKT pathway activation in CN.

a Comparison of the tumor mutation burden ratio of CN with other cancers revealed a low score relative to that of other CNS tumors, such as GBM and LGG. b Pathway analysis of significantly differentially expressed genes in CN compared to that in normal brain samples revealed the PI3K-AKT1 pathway as one of the top upregulated pathways in CN. c Enrichment analysis of significantly overexpressed genes in CN compared to that in normal brain samples. d IHC validation of overexpressed PI3K-AKT pathway marker genes along with FGFR3 in CN (scale bar 100 µM). e Functional classification of the PI3K-AKT1 pathway downstream of GSK3-related genes showed that metabolism-, proliferation-, and survival-related genes were upregulated and that neuronal function-related genes were downregulated in CN. (Asterisks represent the following P values: *<0.05; **<0.01; ***<0.001; ****<0.0001).