Mutation of the p53 tumor-suppressor gene is not a feature of endometrial hyperplasias.

Published

Journal Article

OBJECTIVE: Mutation and overexpression of the p53 gene occur in approximately 20% of endometrial carcinomas. To determine whether alteration of the p53 gene is an early event in endometrial carcinogenesis, we examined the p53 gene in endometrial hyperplasias. STUDY DESIGN: Genomic deoxyribonucleic acid was extracted from 117 endometrial hyperplasias (36 simple, 40 complex, 41 atypical) and 30 endometrial cancers. Exons 5 through 8 of the p53 gene were amplified by means of the polymerase chain reaction. Mutations in the p53 gene were sought with single-stranded conformation polymorphism analysis and confirmed by direct deoxyribonucleic acid sequencing. RESULTS: None of 117 endometrial hyperplasias were found to have mutations in the p53 gene, whereas mutations were seen in three of 30 (10%) endometrial cancers (p < 0.02). The p53 mutations seen in three cancers were confirmed by direct sequencing (codons 157, 180, 272). CONCLUSION: Because it does not appear to be a feature of endometrial hyperplasias, mutation of the p53 gene may represent a relatively late event in endometrial carcinogenesis.

Full Text

Duke Authors

Cited Authors

  • Kohler, MF; Nishii, H; Humphrey, PA; Saski, H; Marks, J; Bast, RC; Clarke-Pearson, DL; Boyd, J; Berchuck, A

Published Date

  • September 1, 1993

Published In

Volume / Issue

  • 169 / 3

Start / End Page

  • 690 - 694

PubMed ID

  • 8372881

Pubmed Central ID

  • 8372881

International Standard Serial Number (ISSN)

  • 0002-9378

Digital Object Identifier (DOI)

  • 10.1016/0002-9378(93)90644-x

Language

  • eng

Conference Location

  • United States