| Research Abstract |
Smooth muscle tumors of the uterus can be divided histologically into benign, malignant, and borderline types. The histological heterogeneity of these smooth muscle tumors suggests that there may be differences in growth potential as well as in growth mechanism among the various types. However, the molecular mechanisms involved in the growth regulation of these tumors are not fully understood. To investigate the cell cycle regulatory machineries involved in the growth mechanism. of smooth muscle tumors, we studied the expression of Ki-67, cyclins E and A, and their catalytic partners, the cyclin-dependent kinases cdk2 and cdc2 using tissue specimens from benign and malignant smooth muscle tumors. These included 20 cases of usual leiomyoma (UL), 18 of cellular leiomyoma (CL), 8 of bizarre leiomyoma (BL), 8 of uncertain malignant potential tumors (UMP.), and 20 of leiomyosarcorna (LMS). The proliferation rate detected by Ki-67 was low in normal myometrium and leiomyomas (UL, CL, and BL), but it was markedly increased in LMS.The expression of the cyclins (E and A), and cdks (cdk2 and cdc2) was also low in normal myometrium and leiomyomas. However, the expression of these factors was markedly increased in LMS.In addition, a survival analysis by Log-rank test revealed that those LMSs with positive staining for cyclin A and with diffusely staining for cyclin E were associated with significantly shorter survival. These results suggest that expression of cyclins and cdks may be involved in the growth control of uterine smooth muscle tumors.
|
