BACKGROUND: Prostatic intraepithelial neoplasia (PIN), an intraluminar proliferation of epithelial cells in ducts and acini, is divided into high-grade (HGPIN) and low-grade (LGPIN), based on morphologies. HGPIN is considered to be a putative precursor of prostatic adenocarcinoma (PCA). Information on PIN has been limited in Japan, because PIN had not been regarded as a precursor lesion for PCA. METHODS: In this study, extent and zonal distribution of PIN together with its relationship with PCA were examined in totally embedded radical prostatectomy specimens obtained from 70 patients with PCA. Fifty-three patients received androgen deprivation therapy (castrated) and remaining 17 did not (noncastrated). RESULTS: Frequency of HGPIN in noncastrated cases (76%) was much higher than that in castrated cases (26%) (P < 0.001). LGPIN showed the same tendency, but the difference was smaller. Difference in mean number of HGPIN in noncastrated and castrated cases (12.0 and 6.4, respectively) was more marked than in LGPIN (6.4 and 5.1, respectively). Reduction rate of mean size in HGPIN (26%) by the androgen deprivation therapy was larger than in LGPIN. When evaluated in noncastrated cases, the coexistence of PCA and HGPIN was found in 76% of cases in the nontransition and 53% in the transition zone. Close association of PCA and PIN (</=2 mm distance between lesions) was more frequently found in HGPIN (55% of lesions) than in LGPIN (37%) (P < 0.05). Frequency of close association of HGPIN with PCA was 65% in the nontransition and 35% in transition zone. CONCLUSIONS: The present study from Japan supports the etiological importance of HGPIN in the development of PCA. The effect of androgen deprivation therapy is much more marked in HGPIN than in LGPIN. Copyright 2000 Wiley-Liss, Inc.
BACKGROUND:Prostatic intraepithelial neoplasia (PIN), an intraluminar proliferation of epithelial cells in ducts and acini, is divided into high-grade (HGPIN) and low-grade (LGPIN), based on morphologies. HGPIN is considered to be a putative precursor of prostatic adenocarcinoma (PCA). Information on PIN has been limited in Japan, because PIN had not been regarded as a precursor lesion for PCA. METHODS: In this study, extent and zonal distribution of PIN together with its relationship with PCA were examined in totally embedded radical prostatectomy specimens obtained from 70 patients with PCA. Fifty-three patients received androgen deprivation therapy (castrated) and remaining 17 did not (noncastrated). RESULTS: Frequency of HGPIN in noncastrated cases (76%) was much higher than that in castrated cases (26%) (P < 0.001). LGPIN showed the same tendency, but the difference was smaller. Difference in mean number of HGPIN in noncastrated and castrated cases (12.0 and 6.4, respectively) was more marked than in LGPIN (6.4 and 5.1, respectively). Reduction rate of mean size in HGPIN (26%) by the androgen deprivation therapy was larger than in LGPIN. When evaluated in noncastrated cases, the coexistence of PCA and HGPIN was found in 76% of cases in the nontransition and 53% in the transition zone. Close association of PCA and PIN (</=2 mm distance between lesions) was more frequently found in HGPIN (55% of lesions) than in LGPIN (37%) (P < 0.05). Frequency of close association of HGPIN with PCA was 65% in the nontransition and 35% in transition zone. CONCLUSIONS: The present study from Japan supports the etiological importance of HGPIN in the development of PCA. The effect of androgen deprivation therapy is much more marked in HGPIN than in LGPIN. Copyright 2000 Wiley-Liss, Inc.