p53 mutations in human malignant gliomas: comparison of loss of heterozygosity with mutation frequency.

Roger H. Frankel, William Bayona, Maxim Koslow, Elizabeth W. Newcomb

PubMed · 1992 · 244 citations · 35 references

Concepts

TL;DR

The study examined p53 mutations in 40 gliomas using SSCP and RFLP to assess loss of heterozygosity at chromosome 17p. p53 mutations were found in 40 % of gliomas, mainly in exons 4–8, with G:C→T:A transversions clustering in exon 5 (codons 156–168) and occurring in >25 % of cases; 37 % of tumors had mutations, rising to 64 % when one 17p allele was lost, yet 36 % of tumors with a single 17p allele lacked p53 mutations, implying another 17p tumor suppressor may drive malignancy.

Abstract

Mutations in the p53 gene were analyzed in 40 gliomas using the single strand conformation polymorphism assay together with restriction fragment length polymorphism analysis to assess loss of heterozygosity for 17p alleles in the same tumors. Mutations occurred in 40% of the gliomas and were found in exons 4-8 of the p53 gene. G:C to T:A transversions, which occur in high frequency in some lung (greater than 50%), liver (greater than 80%), breast (30%), and esophageal cancers (25%), were noted in greater than 25% of the gliomas studied here. These transversions were clustered in exon 5 from codons 156 to 168, a region of the p53 gene not previously associated with a high frequency of mutation, and may represent a new hot spot for mutations in certain cancers. The majority of gliomas (27 of 38) analyzed here retained both 17p alleles. The frequency of p53 mutations was 37% in this group of tumors and increased to 64% in tumors with one 17p allele. Allelic loss for chromosome 17p occurred in 4 of 11 gliomas independently of mutations in the p53 gene. Absence of p53 mutations in 36% of the tumors with one 17p allele suggests that a tumor suppressor gene other than p53 may be located on chromosome 17p and involved in progression to malignancy of some gliomas.

References

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