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

Am J Obstet Gynecol. 1993 Sep;169(3):690-4. doi: 10.1016/0002-9378(93)90644-x.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • DNA, Single-Stranded / chemistry
  • Endometrial Hyperplasia / genetics*
  • Endometrial Neoplasms / genetics
  • Female
  • Genes, p53 / genetics*
  • Humans
  • Molecular Conformation
  • Molecular Sequence Data
  • Mutation*
  • Oligodeoxyribonucleotides / chemistry
  • Polymerase Chain Reaction
  • Polymorphism, Genetic

Substances

  • DNA, Single-Stranded
  • Oligodeoxyribonucleotides