This Tumours accounts for about 25 % of all brain Tumours in children and has an incidence of approximately 1/100,000 per year. Medulloblastoma occurs predominantly in the first two decades of life, with a peak incidence between 3 and 5 years of age. Familial medulloblastoma appears to be uncommon but has been reported in twins and siblings (Hung et al. 1990). Familial non- syndromic medulloblastoma occurs rarely (von Koch et al. 2002). Genetic disorders associated with medulloblastoma include Gorlin syndrome, familial adenomatous polyposis and Turcot syndrome, blue rubber bleb nevus syndrome, and ataxia telangiectasia. Gorlin syndrome is caused by germline mutations in the PTCH gene which encodes the sonic hedgehog receptor. In addition, germline and somatic mutations in another of the sonic hedgehog pathway, SUFU (encoding the human suppressor of fused), may be found in a subset of children with early-onset (before 3 years) medulloblastoma and can be dominantly inherited with incomplete penetrance (Taylor et al. 2002; Brugieres et al. 2010). Medulloblastoma may also occur in patients with homozygous BRCA2 mutations (Fanconi Anaemia Type D1) (Offit et al. 2003; Hirsch et al. 2004).
Cancer genome analysis of medulloblastoma revealed that the most commonly altered genes were implicated in the Hedgehog, Wnt, and histone methylation pathways (Parsons et al. 2011).