Mechanisms of acquired resistance to androgen receptor targeting drugs in castration-resistant prostate cancer

被引：32

作者：

Chism, David D. ^{[1
]}

De Silva, Dinuka ^{[2
]}

Whang, Young E. ^{[1
,2
]}

机构：

[1] Univ N Carolina, Dept Med, Div Hematol & Oncol, Chapel Hill, NC 27599 USA

[2] Univ N Carolina, Dept Pathol & Lab Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

来源：

EXPERT REVIEW OF ANTICANCER THERAPY | 2014年 / 14卷 / 11期

关键词：

abiraterone; acquired drug resistance; androgen receptor; androgen receptor splice variants; enzalutamide; glucocorticoid receptor; intratumoral androgen synthesis; prostate cancer; SPLICE VARIANTS; ABIRATERONE ACETATE; ENZALUTAMIDE MDV3100; ANTITUMOR-ACTIVITY; INCREASED SURVIVAL; CLINICAL ACTIVITY; PLUS PREDNISONE; DOCETAXEL; THERAPY; ANTIANDROGEN;

D O I：

10.1586/14737140.2014.928594

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

After initial response to androgen receptor (AR) targeting drugs abiraterone or enzalutamide, most patients develop progressive disease and therefore, castration resistant prostate cancer remains a terminal disease. Multiple mechanisms underlying acquired resistance have been postulated. Intratumoral androgen synthesis may resume after abiraterone treatment. A point mutation in the ligand-binding domain of AR may confer resistance to enzalutamide. Emergence of AR splice variants lacking the ligand-binding domain may mediate resistance to abiraterone and enzalutamide. Steroid receptors such as glucocorticoid receptor may substitute for AR. Drugs with novel mechanisms of action or combination therapy, along with biomarkers for patient selection, may be needed to improve the therapy of castration resistant prostate cancer.

引用

页码：1369 / 1378

页数：10

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