To further illustrate the roles of p53 gene, epidermal growth factor receptor (EGFR) gene and loss of heterozygosity (LOH) on chromosome 10 and 17?p in human glioma progression Methods p53 mutations were scanned in 50 gliomas with various malignant grades using the polymerase chain reaction single strand conformation polymorphism (PCR SSCP) assay, and were confirmed by direct sequencing LOH for chromosome 10, 17?p and amplification of the EGFR gene were also assessed using Southern blot analysis Results p53 mutations were found in 9 of 17 high grade astrocytomas (53%), 1 of 15 low grade astrocytomas (7%), and the only subject of eppendymoblastoma but in none of the 10 medulloblastomas and 7 eppendymomas The majority of gliomas (38/50) analyzed here retained both 17?p alleles The frequency of p53 mutations was 13% in this group of tumors and increased to 50% (6/12) in tumors with one 17?p allele ( P <0 025) LOH on chromosome 10 was found in 35% (6/17) of high grade astrocytomas, in 10% (1/10) of medulloblastomas, but in 0% of low grade gliomas EGFR gene amplification was found in 9 high grade gliomas, 60% (6/9) of which also presented LOH for chromosome 10 Conclusions 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 To further demonstrate the roles of p53 gene, epidermal growth factor receptor (EGFR) gene and loss of heterozygosity (LOH) on chromosome 10 and 17?p in human glioma progression Methods p53 mutations were scanned in 50 gliomas with various malignant grades using the polymerase The chain reaction single strand conformation polymorphism (PCR SSCP) assay, and were confirmed by direct sequencing LOH for chromosome 10, 17?p and amplification of the EGFR gene were also assessed using Southern blot analysis Results p53 mutations were found in 9 of 17 high grade Astrocytomas (53%), 1 of 15 low grade astrocytomas (7%), and the only subject of eppendymoblastoma but in none of the 10 medulloblastomas and 7 eppendymomas The majority of gliomas (38/50) analyzed hereboth both both?p alleles The frequency of p53 mutations was 13% in this group of tumors and increased to 50% (6/12) in tumors with one 17?p allele (P<0 025) LOH on chromosome 10 was found in 35% (6/17 ) of hi Gh grade astrocytomas, in 10% (1/10) of medulloblastomas, but in 0% of low grade gliomas EGFR gene amplification was found in 9 high grade gliomas, 60% (6/9) of which also presented LOH for chromosome 10 Conclusions 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 The 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