|Budget Amount *help
¥2,100,000 (Direct Cost : ¥2,100,000)
Fiscal Year 1996 : ¥900,000 (Direct Cost : ¥900,000)
Fiscal Year 1995 : ¥1,200,000 (Direct Cost : ¥1,200,000)
To know the difference of growth control mechanism between endometriosis and the endometrium, expression of sex steroid receptors (estrogen receptors : ER,Progesterone receptors : PR), Ki-67, Proliferating cell nuclear antigen (PCNA), G1 cell cycle regulatory molecules (cyclins, cyclin-dependent kinases : CDKs), and tumor suppressor gene product (p53) was analyzed in these tissues. Immunohistochemically, ER, PR, cyclin E, cyclin A,cyclin B,cdk4, cdk2, cdc2, and p53 were stained in 18 endometriotic lesions from 10 patients and in their corresponding normal eutopic endometria. Of the 10 patients, 6 were in the proliferative and 4 were in the secretory phase of the menstrual cycle. The normal eutopic endometrial glands showed the expression of both ER and PR in the proliferative phase and down-expression of these receptors in the secretory phase, and they were negative for p53. Of 18 endometriotic lesions, 13 exhibited both ER and PR staining irrespective of the phases of the menstrual cycle. While 4 showed negative staining for both ER and PR in the epithelial cells and p53 positive cells were intermingled. The expression of Ki-67, PCNA,cyclins and CDKs was observed in both the endometriotic lesions and normal endometria. However, compare to the normal endometrium, PCNA,cyclin E,cyclin A and cdk4 were frequently expressed in the endometriotic lesions of the secretory phase. The expression of sex steroid receptors and G1 cell cycle regulatory molecules in endometriotic lesions was not coordinated with that of the eutopic endometrium. The endometriotic lesions, which showed overexpression of p53 and negative expression of ER and PR,might be in a process of neoplastic transformation.