Expression of Cyclin E and Cyclin-Dependent Kinase Inhibitor, p27KIP1 in Uterine Endometrial Carcinoma: Relationship with p53 Status

Publisher Website
Google Scholar
Abstract
In an effort to clarify the cell-cycle regulator factors that affect the development and growth of endometrial carcinoma, immunohistochemical analyses of cyclin E, p27KIPI, and p53 were performed in 36 cases of endometrial carcinoma (31 endometrioid and five serous carcinomas) and 40 cases of endometrial hyperplasia (20 simple hyperplasia and 20 complex hyperplasia). A correlation of expressions of these regulators with clinicopathologic features was analyzed. Overexpression of cyclin E was found in 0%, 30%, and 52.8% of simple hyperplasia, complex hyperplasia, and endometrial carcinoma, respectively. The p53 was overexpressed in 20%, 25%, and 69.4% of simple hyperplasia, complex hyperplasia, and endometrial carcinoma, respectively. Immunoreactivity of p53 in endometrial carcinoma was significantly higher than in simple and complex hyperplasia (p<.05). The immunoreactive indices of cyclin E and p53 in cases of stage Ic were higher than in cases of stage lb (p=.047, .021, respectively). Immunoreactivity of p27 in endometrial carcinoma was significantly lower than in normal and hyperplastic endometrium (p<.05). There was a significant correlation between expressions of cyclin E and p53 and an inverse correlation between expressions of p27 and p53 (p<.001). These results suggest that the overexpression of cyclin E and p53 and the downregulation of p27 are implicated in the development and early progression of endometrial carcinoma. The results also suggest that regulatory factors have a close relationship with each other in endometrial hyperplasia and carcinoma.