Format

Send to

Choose Destination
See comment in PubMed Commons below
Clin Genitourin Cancer. 2012 Sep;10(3):141-6. doi: 10.1016/j.clgc.2012.03.005. Epub 2012 May 17.

The role of IMiDs alone or in combination in prostate cancer.

Author information

1
Department of Medicine, Division of Hematology/Oncology, Advocate Lutheran General Hospital, Park Ridge, IL 60068, USA. cnabhan@oncmed.net

Abstract

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.

PMID:
22608152
DOI:
10.1016/j.clgc.2012.03.005
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center