Table 2:

Summary of molecular pathology profiling through the Oncomine Comprehensive Assay across 5 samples in the de novo cohort as well as 6 samples from secondary-progressive cohort^{^a}

De Novo (D.N.)/Secondary Progressive (S.P.)	Pathogenic Variants	Variants of Unknown Significance	WHO Grade at Time of Analysis
S.P.	CDKN2A loss CDKN2B loss FANCG splice site deletion MTAP loss TP53 V31L	–	3

S.P.	ARID1 frameshift alteration FBXW7 frameshift deletion	TSC2 in frame insertion CDH1 missense	3

S.P.	NF2 nonsense CDKN2A deletion	–	3

S.P.	MSH2 nonsense TP53 nonsense PTEN frameshift deletion GNAS missense	–	2

S.P.	–	PIK3R1 missense TSC1 missense NOTCH1 missense NF2 missense	2

S.P.	NF2 splice site CDKN2A deletion	–	1

D.N.	BRCA2 frameshift deletion NF2 nonsense	BRCA2 missense	3

D.N.	–	CCND1 amplification RPS6KB1 amplification	3

D.N.	–	ATM missense	3

D.N.	–	–	3

D.N.	–	–	3

Note:—The en dash indicates no mutations found.
↵a Notably, the 6 samples from the secondary-progressive cohort included 1 sample that was WHO grade 1, two samples that were WHO grade 2, and 3 samples that were WHO grade 3 at the time of genetic analysis. Mutations were stratified by clinical significance and categorized as either pathogenic or variants of unknown significance. TERT promoter mutations were not included in this panel.