Recent insights into mechanisms by which prostate cancer becomes castration resistant have allowed better and more rational therapeutic design.
These novel therapies have complemented the modest success that chemotherapy has shown in recent years changing the landscape of this disease and leading to improved outcomes. Angiogenesis and immune deregulation are 2 pathways that have increasingly been shown to lead into castration resistant prostate cancer (CRPC). Thalidmide and lenalidomide are immunomodulatory agents with antiangiogenesis properties that have shown activity in this setting with acceptable safety profile. In this review, we discuss briefly the different mechanisms that render prostate cancer castration resistant and elaborate on thalidomide and lenalidomide data in CRPC after reviewing their theoretic mechanisms of action. This timely review coincides with the identification of newer therapies against CRPC affirming our steady movement toward better disease control.
Written by:
Nabhan C, Petrylak DP. Are you the author?
Department of Medicine, Division of Hematology/Oncology, Advocate Lutheran General Hospital, Park Ridge, IL.
Reference: Clin Genitourin Cancer. 2012 May 16. Epub ahead of print.
doi: 10.1016/j.clgc.2012.03.005
PubMed Abstract
PMID: 22608152
UroToday.com Prostate Cancer Section