CONCLUSIONS P53 and MDM2 mRNA and protein were elevated in endometrial polyps and endometrial adenocarcinoma and their expressions were correlated with clinical staging of endometrial adenocarcinoma.
In addition, the expression of BAF250a was positively correlated with estrogen receptor and negatively correlated with p53 in poorly differentiated endometrial adenocarcinoma.
Five factors prior to NAC (nuclear grade, pretreatment tumor volume, PCNA index, p53 protein expression, and DNA ploidy) were analyzed for correlation with the decrease in tumor volume and histologic response in cervical and endometrial adenocarcinoma, respectively.
Mutation and overexpression of p53 have been described in uterine malignant mixed Müllerian tumours and in endometrial adenocarcinoma, where it has been associated with a poor prognosis.
Effect of estradiol on tumor growth, cell kinetics and p53 oncoprotein expression in human endometrial adenocarcinoma heterotransplanted into nude mice.
Allelic loss, recognized at the polymorphic site in codon 72 of the p53 gene, was detected in 6 of 19 (32%) informative cases of endometrial adenocarcinoma and 1 of 4 (25%) informative cases of endometrial atypical hyperplasia by restriction fragment length polymorphism analysis and by single-strand conformation polymorphism analysis of polymerase chain reaction (PCR)-amplified DNA fragments.
We therefore suggest that alteration of the Rb gene, as well as activation of the Ki-ras gene and alterations of the p53 gene, plays a significant role in the etiology of endometrial adenocarcinoma.