Prostate cancer (PC) is the second most common cause of cancer-related mortality in the United States, with over 40,000 deaths per year (Horst et al., 1995; Jemal et al., 2003). This cancer exhibits a complex, temporally varying natural history (Visakorpi et al., 1995; Fenton et al., 1997; Craft et al., 1999), and metastatic PC is difficult to treat effectively. Virtually all PCs are initially sensitive to androgen receptor (AR)-mediated signaling and respond to AR blockade or androgen withdrawal. Medical or surgical suppression of androgen action is thus standard first-line therapy for non-resectable PC, and most commonly focuses on androgen ablation, that is, reducing the production of testosterone. Testosterone is converted in the prostate to dihydrotestosterone (DHT), which in turn binds to and activates the AR. The activated receptor regulates the transcription of a number of target genes which support and stimulate the growth of prostatic tissue. The clinical benefits of castration depend on the degree to which the tumor is dependent on androgens for growth and survival, but it is not a curative strategy; the disease will eventually alter its biology, becoming hormone-independent (i.e., castration-resistant) and will continue to grow despite ongoing androgen suppression (Agus et al., 1999). In the clinical state model of PC progression (Scher and Heller, 2000), patients who have failed such therapy are distinguished as either non-castrate or castrate based on measured testosterone concentrations in blood, with castration-resistance representing the lethal variant of the disease.
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Zanzonico, P. (2008). Prostate Cancer: 16β-[18F] Fluoro-5α-Dihydrotesterone (FDHT) Whole-Body Positron Emission Tomography. In: Hayat, M.A. (eds) General Methods and Overviews, Lung Carcinoma and Prostate Carcinoma. Methods of Cancer Diagnosis, Therapy, and Prognosis, vol 2. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-8442-3_36
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