These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: p53 mutation, EGFR gene amplification and loss of heterozygosity on chromosome 10, 17 p in human gliomas.
    Author: Jin W, Xu X, Yang T, Hua Z.
    Journal: Chin Med J (Engl); 2000 Jul; 113(7):662-6. PubMed ID: 11776043.
    Abstract:
    OBJECTIVE: 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.
    [Abstract] [Full Text] [Related] [New Search]