Involvement of the abnormality of cyclins, cyclin-dependent kinases or tumor suppressor gene products in the acquisition of the malignant potential of the endometrial carcinomas.

细胞周期蛋白、细胞周期蛋白依赖性激酶(CDKs)和肿瘤抑制基因产物的相互作用在细胞周期进程中是必不可少的，而这些因子的错乱表达被认为是引起细胞恶性转化的原因。为阐明子宫内膜癌的发生发展过程，采用免疫组织化学方法检测了细胞周期相关分子在正常和恶性子宫内膜组织中的表达。在正常子宫内膜中，细胞周期蛋白A、细胞周期蛋白B1、细胞周期蛋白E、细胞周期蛋白cdc2、细胞周期蛋白cdk2、细胞周期蛋白p16在增生期子宫内膜腺上皮中有零星表达。在子宫内膜癌组织中，Cyclin A、Cyclin B1、Cyclin D1、Cyclin E、CDC2、CDK2、CDK4、P53、P16和Rb的阳性表达例数分别为11、32、22、41、43、32、8、22、39和32例。Cyclin D1、Cyclin A和P53阳性细胞的形态分布相互关联。以上病例分为两组。第一组为只表达Cyclin E的病例，第二组为表达Cyclin D1、P53和Cyclin A的病例，第一组倾向于高分化病例，第二组为低分化病例。这些发现表明，细胞周期相关因子的异常积累参与了子宫内膜癌恶性潜能的获得。

Interactions of cyclins, cyclin-dependent kinases (cdks) and tumor suppressor gene products are essential in cell cycle progression, and deranged expression of these factors are reported to evoke malignant transformation of the cell. To elucidate the tumorigenetic process of the endometrial carcinomas, expression of the cell cycle related molecules in normal and malignant endometrial tissues was investigated by immunostaining. In the normal endometrium, expression of cyclin A, cyclin B1, cyclin E, cdc2, cdk2 and p16 was sporadically observed in the glandular epithelia of the proliferative phase. In 64 cases of endometrial carcinomas, the number of positive cases for cyclin A, cyclin B1, cyclin D1, cyclin E, cdc2, cdk2, cdk4, p53, P16 and RB was 11, 32, 22, 41, 43, 32, 8, 22, 39, and 32 cases, respectively. The topographical distribution of cyclin D1, cyclin A and p53 positive cells correlated each other. Above 64 cases were classified into two groups. The first group was consisted of the cases showing positive for only cyclin E, and the second group was consisted of those expressing cyclin D1, p53 and cyclin A. The first group tended to contain well differentiated cases, and poorly differentiated cases were more frequently found in the second group. These findings suggest that accumulations of abnormalities of the cell cycle related factors are involved in the acquisition of the malignant potential of the endometrial carcinomas.