Therapeutic impact of mTERT-based ACT on TRAMP mice. (A) Activated CTLs are able to traffic to prostate tumor. TRAMP mice were subjected to 3 consecutive ACTs and, 4 days after last ACT, prostate tumors were harvested and stained to track either mTERT-specific (CD8⁺/Vβ11⁺) or β-gal–specific(CD8⁺/Vβ8.1⁺) CTLs. IFN-γ and CD8 staining is shown on cells gated for specific Vβ expression. Data are mean ± SD of 3 mice. (B) Representative histologic pictures of prostates of TRAMP mice treated with either mTERT_198-205–specific (left) or control CTLs (right) at 24 weeks of age. Prostate in majority of mTERT-specific CTL treated mice is occupied by PIN-LG foci, showing normal sized glands lined by few and flat layers of atypical cells. In control mice, PIN-HG–affected prostatic ductules appear enlarged and distorted by crowded intraluminal papillae coalescing into cribriform structures (arrowheads). Numerous solid nests of adenocarcinoma (arrows) focally invade base membrane (see also insert; magnification: top panels, ×200; bottom panels, ×400). The table summarizes the prostate areas occupied by different tumor lesions. Values are expressed as mean ± SE. The incidence of PDC also is indicated. Wilcoxon rank sum test: PIN-LG is more represented in TERT-specific CTL-treated animals (P = .001); PIN-HG is not statistically different; adenocarcinoma (ADC) is more represented in β-gal–specific CTL-treated mice (P = .001). The incidence of PDC was evaluated with the Fisher exact test (P = .001). (C) Overall survival of TRAMP mice undergoing ACT. Survival curves from TRAMP mice treated with either mTERT-specific (n = 9) or β-gal–specific (n = 10) CTLs are shown. Kaplan-Meier analysis: mTERT vs β-gal, P < .001.