DETERMINATION OF P53 MUTATIONS, EGFR OVEREXPRESSION, AND LOSS OF P16 EXPRESSION IN PEDIATRIC GLIOBLASTOMAS

Glioblastoma multiforme is a rare neoplasm in children and is often lo cated infratentorially, particularly in the brainstem. Pediatric gliob lastomas arise frequently (here 60%) outside the cerebral hemispheres. We investigated 20 pediatric glioblastomas for mutational inactivatio n of the p53 tumor suppressor gent, loss of p16 protein expression and overexpression of the epidermal growth factor receptor (EGFR). Mutati ons in the p53 gene were identified in 5/20 (25%) glioblastomas, 4 of which occurred in primary glioblastomas with a clinical history of les s than 4 months and neither clinical nor histologic evidence of a less malignant precursor lesion. Loss of p16 expression was detected in 11 /18 (61%) glioblastomas. Overexpression of the EGFR was infrequent (2/ 19, 11%) and included 1 tumor with a p53 mutation. Of 4 secondary glio blastomas that progressed from histologically diagnosed lower grade tu mors, one contained a p53 mutation. Our results are at variance with s imilar studies in adult patients in which primary and secondary gliobl astomas are characterized by EGFR overexpression and p53 mutations, re spectively, suggesting that the evolution of pediatric glioblastomas f ollows different genetic pathways.