Mutation of the p53 tumor-suppressor gene is not a feature of endometrial hyperplasias.
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.
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Related Subject Headings
- Polymorphism, Genetic
- Polymerase Chain Reaction
- Oligodeoxyribonucleotides
- Obstetrics & Reproductive Medicine
- Mutation
- Molecular Sequence Data
- Molecular Conformation
- Humans
- Genes, p53
- Female
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Polymorphism, Genetic
- Polymerase Chain Reaction
- Oligodeoxyribonucleotides
- Obstetrics & Reproductive Medicine
- Mutation
- Molecular Sequence Data
- Molecular Conformation
- Humans
- Genes, p53
- Female