Ohtani K
Department of Obstetrics and Gynecology, Nihon University School of Medicine, Tokyo.
Nihon Sanka Fujinka Gakkai Zasshi. 1990 Jun;42(6):579-85.
In the present study 18 cases of malignant ovarian neoplasm were studied to determine the possible role of sex steroid hormones and gonadotropins on tumor development. Twelve cases of serous cystadenocarcinoma, 2 of mucinous cystadenocarcinoma, 2 of endometrioid carcinoma, one malignant Brenner tumor, and one yolk sac tumor were examined with respect to their response to estradiol (E2), [D-Ser(But)6]-LHRH (1-9) nonapeptide-etylamide (Buserelin), human menopausal gonadotropin (HMG), RU 38486 (RU), and pure FSH by subrenal capsule assay (SRCA). Also 125I-FSH binding assay and the protein kinase C (CK) activity were studied in vitro. The results showed; 1) Seventy-three% cases showed a significant increase (p less than 0.05) in size due to SRCA. 2) In the FSH, HMG, and Buserelin treated groups, the size of xenografts increased (p less than 0.05) and the highest response was obtained with FSH. 3) Ninety-one% of cases demonstrated in vitro FSH specific binding which was significantly higher (p less than 0.05) in the cases which responded to gonadotropins in SRCA (42,288 +/- 25,454 vs 6,980 +/- 1,952, mean +/- SD, cpm/mg tissue). 4) CK activity was increased significantly (p less than 0.05) by gonadotropin (204.5 +/- 2.4 vs 363.9 +/- 7.2, mean +/- SD, cpm/mg tissue). These results suggest that gonadotropins possibly play a role in prompting the tumorigenesis of the malignant ovarian neoplasms through specific receptors and this mechanism may modify the CK system in malignant ovarian neoplasms.
在本研究中,对18例卵巢恶性肿瘤患者进行了研究,以确定性甾体激素和促性腺激素在肿瘤发生发展中的可能作用。对12例浆液性囊腺癌、2例黏液性囊腺癌、2例子宫内膜样癌、1例恶性勃勒纳瘤和1例卵黄囊瘤,通过肾包膜下移植试验(SRCA)检测了它们对雌二醇(E2)、[D-丝氨酸(叔丁基)6]-LHRH(1-9)九肽-乙基酰胺(布舍瑞林)、人绝经期促性腺激素(HMG)、RU 38486(RU)和纯促卵泡激素(FSH)的反应。同时还进行了体外125I-FSH结合试验和蛋白激酶C(CK)活性研究。结果显示:1)73%的病例经SRCA后肿瘤体积显著增大(p<0.05)。2)在FSH、HMG和布舍瑞林治疗组中,异种移植瘤体积增大(p<0.05),其中FSH的反应最强。3)91%的病例表现出体外FSH特异性结合,在SRCA中对促性腺激素有反应的病例中,其结合水平显著更高(p<0.05)(42,288±25,454对6,980±1,952,平均值±标准差,cpm/mg组织)。4)促性腺激素使CK活性显著升高(p<0.05)(204.5±2.4对363.9±7.2,平均值±标准差,cpm/mg组织)。这些结果提示,促性腺激素可能通过特异性受体在卵巢恶性肿瘤的发生发展中起作用,且这一机制可能改变卵巢恶性肿瘤中的CK系统。