1.1. Overview of prostate cancer and standard treatments

The estimated number of new prostate cancer cases for 2011 was 240,890. The majority of diagnosed prostate cancers (PCa) is found early due to the widespread use of the screening test for prostate specific antigen (PSA) and are considered low risk [1]. The prognosis for men diagnosed with low-risk prostate cancer is good and the NIH is recommending active surveillance [1]. Active surveillance has the benefit of reducing treatment side effects, including erectile dysfunction and incontinence, for men that are unlikely to die from their cancer [2]. Locally advanced prostate cancers are higher risk, and a substantial fraction of these patients will eventually die of the disease, though median survival may be as long as 5 years. If prostate cancer has spread to distant organs, current therapy will inevitably fail [3]. Because the androgen receptor (AR) is important for prostate cancer development and progression, androgen deprivation therapy (ADT), which either reduces the production of an-drogens by surgical or medical castration, or interferes with AR function via the use of anti-androgens, is increasingly becoming a central component in the management of metastatic prostate cancer [3]. ADT initially leads to improved clinical outcomes in about 90% of the cases. However, most tumors become androgen independent (AI) and no longer respond to standard hormonal therapies, chemotherapeutics or radiotherapy [3]. Thus, improved therapeutic strategies that target key pathways and molecules are essential to improve the outcome for patients with AI prostate cancer (AIPC). Interestingly, recent data shows that the AR pathway is often still engaged in AIPC, possibly due to receptor promiscuity or hyper-sensitivity. Therefore, some scientists believe that a strategy of targeting AR expression, ei ther directly or indirectly, may be helpful in these cases [4]. Indeed, elegant methods employing genome wide analysis are being used to identify small molecule antagonists of AR function [5]. Other ideas for targeted therapies include small molecule inhibition of metabolic enzymes such as fatty acid synthase (FASN) because cancer cells, unlike their normal counterparts, synthesize de novo large quantities of fatty acids and cholesterol [6] and inhibitors of vascular endothelial growth factor receptor (VEGFR) to suppress vascularization [7].

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