期刊
CURRENT CANCER DRUG TARGETS
卷 13, 期 4, 页码 444-459出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/15680096113139990078
关键词
Androgen receptor; castration-resistant prostate cancer; docetaxel; prostate cancer
类别
资金
- Kakenhi [22591769, 24890160]
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Takeda Science Foundation, Japan
- Uehara Memorial Foundation to MS, Japan
- Grants-in-Aid for Scientific Research [24890160] Funding Source: KAKEN
Until 2010 docetaxel was the only agent with a proven survival benefit in the treatment of castration-resistant prostate cancer (CRPC). Recent evidence suggests that CRPC is caused by augmented androgen/ androgen receptor (AR) signaling involving AR hypersensitivity, promiscuous activation of the AR, de novo production of androgens and activation of the AR by cytokines and growth factors; these findings have led to the development of novel agents targeting AR signaling. Several novel drugs targeting the AR axis, including the cytochrome P17 inhibitor abiraterone acetate and anti-androgen enzalutamide (MDV3100), have shown promising results in prolonging survival in clinical trials in a post-chemotherapy setting. Because of these encouraging findings, these drugs have also been evaluated in a pre-chemotherapy setting. In addition, several novel drugs targeting non-AR signaling, including the novel taxoid compound cabazitaxel, antisense oligonucleotide OGX-011 (custirsen), sipuleucel-T immunotherapy and Alpharadin-based radiotherapy, have also been demonstrated to improve overall survival in CRPC. However, there is no consensus with regard to the sequence in which these novel drugs and taxanes should be used in the treatment of CRPC. In this review, we summarize recently developed and developing novel agents for use against CRPC. We also discuss the sequence of use of these agents and taxanes, mainly from the standpoint of factors related to drug resistance.
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