Cancer Prevention Research 2, 518, June 1, 2009. Published Online First June 2, 2009;
doi: 10.1158/1940-6207.CAPR-08-0241
© 2009 American Association for Cancer Research
Molecular Profiles of Finasteride Effects on Prostate Carcinogenesis
Jin Li1 and
Jeri Kim2
Authors' Affiliations: Departments of 1 Systems Biology and 2 Genitourinary Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas
Requests for reprints: Jeri Kim, Department of Genitourinary Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Unit 1374, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: 713-792-2830; Fax: 713-745-1625; E-mail: jekim{at}mdanderson.org.
Our inability to distinguish between low-grade prostate cancers that pose no threat and those that can kill compels newly diagnosed early prostate cancer patients to make decisions that may negatively affect their lives needlessly for years afterward. To reliably stratify patients into different risk categories and apply appropriate treatment, we need a better molecular understanding of prostate cancer progression. Androgen ablation therapy and 5-
reductase inhibitors reduce dihydrotestosterone levels and increase apoptosis. Because of the differing biological potentials of tumor cells, however, these treatments may, in some cases, worsen outcome by selecting for or inducing adaptation of stronger androgen receptor signaling pathways. Reduced dihydrotestosterone also may be associated with altered survival pathways. Complicating treatment effects further, molecular adaptation may be accelerated by interactions between epithelial and stromal cells. The hypothesis that early prostate cancer cells with differing biological potential may respond differently to finasteride treatment is worth testing. Ongoing studies using a systems biology approach in a preoperative prostate cancer setting are testing this hypothesis toward developing more-rational clinical interventions.
Copyright © 2009 by the American Association for Cancer Research.
