p53 mutation, EGFR gene amplification and loss of heterozygosity on chromosome 10, 17 p in human gliomas.

Abstract

These results indicate that p53 inactivation is a common genetic event in astrocytoma progression that may be more strongly associated with the progression of astrocytomas than with their origin. Absence of p53 mutations in 50% of the tumors with one 17 p allele suggests that a tumor suppressor gene other than p53 may be located on chromosome 17 p and involved in progression to malignancy of some gliomas. The loss of alleles on chromosome 10 and the amplification of the EGFR gene appear to be restricted to high-grade tumors, suggesting that these events may be related to tumor progression rather than initiation.