Biology of castration-recurrent prostate cancer.
Although androgen-deprivation therapy is the standard therapy for advanced and metastatic prostate cancer, this treatment is only palliative. Prostate cancer recurs then grows despite low circulating testicular androgens, using several mechanisms that remain dependent on androgen-receptor signaling in most cases. This article reviews the diversity of mechanisms used for growth by castration-recurrent prostate cancer.
Department of Urology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. faris.azzouni@roswellpark.org
Faris
F
Azzouni
James
J
Mohler
D000726:Androgen Antagonists / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000494:pharmacology; D005784:Gene Amplification; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D006801:Humans; D008297:Male; D009364:Neoplasm Recurrence, Local / Q000473:pathology / Q000503:physiopathology*; D009376:Neoplasms, Hormone-Dependent / Q000503:physiopathology*; D011467:Prostate / Q000737:chemistry; D011471:Prostatic Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D020033:Protein Isoforms / Q000502:physiology; D011944:Receptors, Androgen / Q000096:biosynthesis / Q000187:drug effects / Q000502:physiology*; D013739:Testosterone / Q000096:biosynthesis; D015533:Transcriptional Activation / Q000502:physiology
D000726:Androgen Antagonists; D000970:Antineoplastic Agents; D020033:Protein Isoforms; D011944:Receptors, Androgen; D013739:Testosterone