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p53 Mutations in Human Malignant Gliomas: Comparison of Loss of Heterozygosity with Mutation Frequency¹

New York University School of Medicine [R. H. F.], Departments of Pathology [W. B., E. W. N.] and Neurosurgery [M. K.], New York University and Kaplan Cancer Center, New York, New York 10016

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 (>50%), liver (>80%), breast (30%), and esophageal cancers (25%), were noted in >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.

¹ This work was supported in part by NIH Grants 5T35DK07421 and P30-16087 and by National Cancer Institute Grant CA 40533.

² To whom requests for reprints should be addressed, at Department of Pathology and Kaplan Cancer Center, New York University Medical Center, 550 First Avenue, New York, NY 10016.

Received 8/30/91. Accepted 1/ 8/92.

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