前列腺癌
恩扎鲁胺
雄激素受体
氟他胺
雄激素
雄激素剥夺疗法
癌症研究
医学
内科学
雄激素受体拮抗剂
抗雄激素
睾酮(贴片)
内分泌学
LNCaP公司
抗雄激素
二氢睾酮
阉割
比卡鲁胺
醋酸阿比特龙酯
前列腺
癌症
激素
作者
Changcheng Guo,Shuyuan Yeh,Yuanjie Niu,Gonghui Li,Junhua Zheng,Lei Li,Chawnshang Chang
出处
期刊:Cancer Letters
[Elsevier BV]
日期:2017-07-01
卷期号:397: 133-143
被引量:29
标识
DOI:10.1016/j.canlet.2017.03.022
摘要
Prostate cancer (PCa) is the 2nd leading cause of cancer-related death among men in the United States and its progression is tightly associated with the androgen/androgen receptor (AR) signals. Men castrated before puberty (eunuchs) or men with inherited deficiency of type II 5α-reductase (with failure to convert testosterone to the more potent dihydrotestosterone) (DHT) do not develop PCa. To date, androgen deprivation therapy (ADT) with anti-androgen treatments to reduce or prevent androgens from binding to the AR remains the main therapeutic option for advanced PCa since its discovery by Huggins and Hodges in 1941. Multiple strategies related to surgical/chemical castration with combinations of various anti-androgens, including Cyproterone Acetate, Flutamide, Nilutamide, Bicalutamide (Casodex) and Enzalutamide, as well as some androgen synthesis blockers, including Abiraterone, have been used to control PCa progression. However, patients on ADT with anti-androgen treatment eventually develop resistance, which might be accompanied with the unwanted side effects of enhanced metastasis. New therapeutic approaches via directly targeting the AR with ASC-J9®, Cisplatin, EPI-001, Niclosamide, and VPC compounds as well as silencing AR with siRNAs or non-coding RNAs have been developed to further suppress PCa at the castration resistant stages.
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