Antiprogestins in gynecological diseases.
Antiprogestins in gynecological diseases.
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DOI：
10.1530/rep-14-0416
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发表时间：
2015-01
期刊：
影响因子：
--
通讯作者：
Telleria CM
中科院分区：
文献类型：
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作者：
Goyeneche AA;Telleria CM
抗孕激素是一组自20世纪80年代初发展起来的化合物，它们以不同的亲和力结合孕激素受体。抗黄体酮的最初临床用途是生殖医学，例如调节月经、紧急避孕和终止早孕。然而，这些最初的应用掩盖了这些化合物干扰细胞生长的能力。在妇科疾病的情况下，抗孕激素可以阻止和杀死与妇科有关的癌细胞，如那些起源于乳房、卵巢、子宫内膜和子宫颈的癌细胞。它们还可以阻断细胞的过度生长，从而导致良性妇科疾病，如子宫内膜异位症和平滑肌瘤（子宫肌瘤）。本文就抗孕激素对多种妇科疾病细胞的抗生长作用的相关文献进行综述。我们还提供了一个总结的细胞和分子机制报道这些化合物，导致细胞生长抑制和死亡。在过去几年中获得的临床前知识为鼓励使用抗孕激素以减轻妇科疾病的负担提供了强有力的证据，无论是作为单一疗法还是作为其他疗法的辅助疗法，都可以允许副作用可耐受的长期治疗。抗黄体酮在这一领域取得临床成功的关键可能在于选择那些将从这种治疗中受益的患者。这可以通过定义所需的基因组成来实现——在每个特定的妇科疾病中——以获得抗孕激素驱动的生长抑制治疗的客观反应。该摘要的西班牙语译本可在http://www.reproduction-online.org/content/149/1/15/suppl/DC1免费获得。
Antiprogestins constitute a group of compounds, developed since the early 1980s, that bind progesterone receptors with different affinities. The first clinical uses for antiprogestins were in reproductive medicine, e.g., menstrual regulation, emergency contraception, and termination of early pregnancies. These initial applications, however, belied the capacity for these compounds to interfere with cell growth. Within the context of gynecological diseases, antiprogestins can block the growth of and kill gynecological-related cancer cells, such as those originating in the breast, ovary, endometrium, and cervix. They can also interrupt the excessive growth of cells giving rise to benign gynecological diseases such as endometriosis and leiomyomata (uterine fibroids). In this article, we present a review of the literature providing support for the antigrowth activity that antiprogestins impose on cells in various gynecological diseases. We also provide a summary of the cellular and molecular mechanisms reported for these compounds that lead to cell growth inhibition and death. The preclinical knowledge gained during the past few years provides robust evidence to encourage the use of antiprogestins in order to alleviate the burden of gynecological diseases, either as monotherapies or as adjuvants of other therapies with the perspective of allowing for long-term treatments with tolerable side effects. The key to the clinical success of antiprogestins in this field probably lies in selecting those patients who will benefit from this therapy. This can be achieved by defining the genetic makeup required – within each particular gynecological disease – for attaining an objective response to antiprogestin-driven growth inhibition therapy. A Spanish translation of this abstract is freely available at http://www.reproduction-online.org/content/149/1/15/suppl/DC1.