Table 2.

Medulloblastoma subgroups with relevant clinical, molecular information and risk stratification.

Subgroup	WNT-activated	SHH-activated (TP53 wildtype and mutated)	Group 3	Group 4(non-WNT, non-SHH)
Clinical Information
Age at diagnosis	Child > 4 years old, adolescents and adults	Bimodal, most often occurring in infants and adults	Infants and young children	Childhood and adolescents
Anatomic location	Midline with involvement of brainstem or in cerebellar peduncle and cerebellopontine angle cistern	Cerebellar hemispheres	Midline vermian location adjacent to 4th ventricle	Midline vermian
Histology	Classic, rarely LCA	Desmoplastic/nodular, Classic, LCA	Classic, LCA	Classic, LCA
Molecular characteristics
Recurrent gene amplifications		MYCN* GLI1 or GLI2*	MYC* MYCN* OTX2	SNCAIP MYCN* OTX2 CDK6
Recurrent single-nucleotide variants/mutations	CTNNB1 DDX3X SMARCA4 TP53 CSNK2B	PTCH1 TERT** SUFU* SMO** TP53 U1 snRNA** DDX3X**	SMARCA4 KBTBD4 CTDNEP1 KMT2D	KDM6A SMYM3 KTM2C KBTBD4
Cytogenetic events	Loss of chromosome 6*	Gain of chromosome 3q or 9p Loss of chromosome 3p, 9q, 10q, 14q, 17p	Gain of chromosome 1q Loss of chromosome 8, 10q,11, 16q Isochromosome 17q	Gain of chromosome 7, 18q Loss of chromosome 8, 11, 13q Isochromosome 17q
Outcome Predictors
Childhood	nuclear B-catenin accumulation#	TP53 mutations##	MYC amplification##	Chromosome 8 loss# Amplification of MYC or MYCN ##
Adult		10q, 3p, or 17p loss## PTCH1 mutations## TP53 mutations##	Isochromosome 17q##	Chromosome 8 loss # CDK6## Isochromosome 17q##

LCA, Large cell anaplastic; *more likely to be associated with childhood medulloblastoma, **more likely to be associated with adult medulloblastoma, # associated with better prognosis, ## associated with inferior prognosis.