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. Author manuscript; available in PMC: 2014 Jan 1.
Published in final edited form as: Cancer Discov. 2012 Dec 20;3(1):44–51. doi: 10.1158/2159-8290.CD-12-0262

Fig. 1. Androgen deprivation potentiated the disease progression from HG-PIN to invasive CRPC.

Fig. 1

(a) Genetic ablation of PTEN in prostatic epithelium caused HG-PIN. IF: pAKT/SMA. (b) Surgical castration induced extensive apoptosis in HG-PIN lesions (left, IF: TUNEL), whereas a subpopulation of tumor cells continued to proliferate (right, IHC: anti-BrdU). (c) PTEN-null prostate tumor mass initially shrank in response to surgical castration but gradually grew back. (d) Androgen deprivation accelerated progression of PTEN-null HG-PIN to invasive CRPC, arrows indicating invasive lesions. Shown are representative lesions observed in 30/32 (93.75%) mice. IHC: anti-SMA. (e) AR staining in CRPC vs. castration naïve HG-PIN. IHC: anti-AR. (f) Western blot of p53 and AR in age-matched wide-type prostate (WT), HG-PIN and CRPC. (g) Chemical castration accelerated progression of PTEN-null HG-PIN to invasive CRPC, arrows indicating invasive lesions. Shown are representative lesions observed in 8/10 (80%) mice. IHC: anti-SMA. Mice harboring HG-PIN at 8 weeks of age were surgically or chemically castrated for another 16–18 weeks, representative data are shown in Fig. 1d, Fig. 1e, Fig. 1f and Fig. 1g. (h) A comparison between the clinical and preclinical trials over the time. High-grade cancer is seen in human trials, whereas invasive CRPC is evident in the preclinical mouse studies.