TY - JOUR
T1 - Mutation of the p53 tumor-suppressor gene is not a feature of endometrial hyperplasias
AU - Kohler, Matthew F.
AU - Nishii, Hiroshi
AU - Humphrey, Peter A.
AU - Saski, Hiroshi
AU - Marks, Jeffrey
AU - Bast, Robert C.
AU - Clarke-pearson, Daniel L.
AU - Boyd, Jeff
AU - Berchuck, Andrew
N1 - Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 1993/9
Y1 - 1993/9
N2 - 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.
AB - 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.
KW - endometrial hyperplasia
KW - p53
KW - tumor-suppressor gene
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U2 - 10.1016/0002-9378(93)90644-X
DO - 10.1016/0002-9378(93)90644-X
M3 - Article
C2 - 8372881
AN - SCOPUS:0027377495
SN - 0002-9378
VL - 169
SP - 690
EP - 694
JO - American journal of obstetrics and gynecology
JF - American journal of obstetrics and gynecology
IS - 3
ER -