Testosterone secretion by cultured arrhenoblastoma cells: suppression by a luteinizing hormone-releasing hormone agonist.
Testosterone secretion by cultured arrhenoblastoma cells: suppression by a luteinizing hormone-releasing hormone agonist.
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培养的成肾细胞瘤细胞分泌睾酮：黄体生成素释放激素激动剂抑制。
DOI：
10.1210/jcem-54-2-450
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
F. de Jong
中科院分区：
文献类型：
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作者：
S. Lamberts;J. Timmers;R. Oosterom;T. Verleun;F. de Jong
对一例男性化患者进行了研究。基础尿17-酮类固醇排泄量在正常上限，但血浆睾酮浓度显著升高。睾酮的分泌可被hCG刺激，被地塞米松抑制，而不受ACTH的影响。手术中发现左侧卵巢的卵巢母细胞瘤，分离培养的肿瘤细胞分泌睾酮。加入LRH激动剂（10 ng/ml）可使睾酮分泌抑制50%（P <0.01）。LRH激动剂对类固醇生成的抑制作用表明，LRH受体存在于该肿瘤上，并且用LRH激动剂治疗转移性类固醇激素分泌性卵巢和睾丸肿瘤患者可能是有益的。
A patient with virilization was studied. The basal urinary excretion of 17-ketosteroids was at the upper limit of normal, but the plasma testosterone concentration was greatly elevated. Testosterone secretion could be stimulated by hCG, suppressed by dexamethasone, and was not affected by ACTH. At operation, an arrhenoblastoma of the left ovary was found. Isolated tumor cells in culture secreted testosterone. The addition of a LRH agonist (10 ng/ml) suppressed the secretion of testosterone by 50% (P less than 0.01). The inhibiting effect of a LRH agonist on steroidogenesis suggests that LRH receptors were present on this tumor and that treatment with LRH agonists might be beneficial in patients with metastatic steroid hormone-secreting ovarian and testicular tumors.