Endogenous hormones and ovarian cancer: epidemiology and current hypotheses.
Endogenous hormones and ovarian cancer: epidemiology and current hypotheses.
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DOI：
10.1158/1055-9965.98.14.1
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发表时间：
2005-01
期刊：
影响因子：
--
通讯作者：
A. Lukanova;R. Kaaks
中科院分区：
文献类型：
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作者：
A. Lukanova;R. Kaaks
根据几种激素假说，包括促性腺激素、雄激素、黄体酮、雌激素、胰岛素样生长因子-I 和胰岛素假说，对卵巢癌主要流行病学危险因素的影响进行了回顾。还简要概述了包涵囊肿形成和苗勒管上皮分化在该疾病病理学中的作用。尽管基于有限的数据，但当前证据中观察到的趋势表明雄激素和雌激素升高以及孕激素降低在卵巢癌的发病机制中可能具有病因作用。不能完全排除促性腺激素的直接作用，但它们对卵巢癌风险的影响可能是通过刺激卵巢类固醇生成介导的。胰岛素样生长因子-I 也作为一种激素出现，可能直接参与该疾病的发病机制，但迄今为止只有一项前瞻性研究检验了这种关联。高胰岛素血症不太可能是卵巢癌的危险因素。观察到的卵巢来源雄激素（绝经前女性）风险增加的趋势，与肾上腺雄激素缺乏关联，以及观察到的与肥胖、激素替代疗法的使用和绝经后内源性激素的相对较弱的关联表明，性类固醇的卵巢合成而不是其循环水平可能在病因学上很重要。来自前瞻性研究的更多数据对于提高我们对内源性激素在卵巢癌发病机制中的病因作用的理解至关重要。这些数据最终将为有针对性的研究提供机会；及早发现和预防性干预。
The effect of major epidemiologic risk factors for ovarian cancer has been reviewed in the light of several hormonal hypotheses, including the gonadotropin, androgens, progesterone, estrogens, insulin-like growth factor-I, and insulin hypotheses. The role of inclusion cyst formation and Mullerian epithelium differentiation in the pathology of the disease are also briefly outlined. Although based on limited data, the observed tendency in current evidence suggests possible etiologic roles for elevated androgens and estrogens and decreased progesterone in the pathogenesis of ovarian cancer. A direct effect of gonadotropins cannot be entirely ruled out, but it is plausible that their effect on ovarian cancer risk is mediated by stimulation of ovarian steroidogenesis. Insulin-like growth factor-I also emerges as a hormone that may be directly involved in the pathogenesis of the disease, but thus far only one prospective study has examined this association. Hyperinsulinemia is an unlikely risk factor for ovarian cancer. The observed tendency for an increased risk with androgens from ovarian origin (in premenopausal women), the lack of association with adrenal androgens, and the relatively weak associations observed with obesity, hormonal replacement therapy use, and endogenous hormones after menopause suggest that ovarian synthesis of sex steroids rather than their circulating levels may be etiologically important. More data from prospective studies will be crucial to improve our understanding of the etiologic role of endogenous hormones in the pathogenesis of ovarian cancer. Such data will ultimately provide opportunities for research targeted; at early detection and preventive interventions.