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Does benign prostatic hyperplasia originate from the peripheral zone of the prostate? A preliminary study
Author(s) -
Tang Jie,
Yang Jing Chun,
Zhang Yan,
Liu Xin,
Zhang Lihai,
Wang Zhili,
Li Junlai,
Luo Yukun,
Xu Jianhong,
Shi Huaiyin
Publication year - 2007
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/j.1464-410x.2007.07081.x
Subject(s) - stromal cell , hyperplasia , pathology , immunohistochemistry , prostate , stroma , epithelium , immunostaining , biopsy , proliferative index , androgen receptor , apoptosis , proliferation index , biology , medicine , prostate cancer , cancer , biochemistry
OBJECTIVE To compare the histological characteristics, cell proliferation, apoptosis and biological features in benign prostatic hyperplasia (BPH) in the peripheral (PZ) and transition zone (TZ) of the prostate. PATIENTS AND METHODS Tissue from BPH in TZ and PZ was obtained from 68 patients undergoing transrectal ultrasonography‐guided biopsy and used for both morphometric analysis and immunohistochemical studies. The epithelial, stromal and luminal composition of the tissue was determined using a computer‐assisted method for quantitative morphometric analysis. Apoptosis was detected as the apoptotic index (AI) using the TdT dUTP nick‐end labelling assay. Cell proliferation was determined as the proliferation index (PI) using Ki‐67 immunostaining. The expression of epidermal growth factor receptor (EGFR), transforming growth factor β1 (TGFβ1), androgen receptor (AR) and bcl‐2 were assessed immunohistochemically. RESULTS There was no difference in the stroma/epithelium ratio between PZ and TZ hyperplastic nodules ( P > 0.05). The mean AI in epithelium was almost identical to the corresponding PI. In stroma, no apoptotic cells were detectable. There was a significantly higher PI and AI in the glandular epithelial cells in PZ hyperplastic than in TZ hyperplastic nodules, but no difference in PI of the stromal cells between PZ and TZ hyperplastic nodules. There was significantly higher expression of TGFβ1 and lower expression of EGFR and bcl‐2 in PZ than TZ hyperplastic nodules ( P < 0.05). There was no difference in AR expression between PZ and TZ hyperplastic nodules ( P > 0.05). CONCLUSIONS These results indicate that some hyperplastic nodules in PZ might originate from the PZ, and the formation of these nodules might be modulated in a different way from that in the TZ.