期刊
CANCER LETTERS
卷 397, 期 -, 页码 133-143出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2017.03.022
关键词
AR degradation; AR splicing variant; Anti-androgen; Castration resistant prostate cancer; Combination therapy
类别
资金
- NIH [CA155477, CA156700]
- George Whipple Professorship Endowment
- Taiwan Department of Health Clinical Trial, Research Center of Excellence [DOH99-TD-B-111-004]
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 5 alpha-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 (R), 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. Published by Elsevier Ireland Ltd.
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