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From the Institute of Pathology, University of the Saarland, Homburg/Saar, Germany
Estrogens have been implicated in prostatic cancerogenesis and
tumor progression. The mechanisms underlying estrogen signaling in
human prostate tissue, however, remain poorly
understood. Using immunohistochemical and in situ
hybridization (ISH) techniques, the present study demonstrates
the classical estrogen receptor (ER
) in premalignant lesions and
prostatic adenocarcinoma through the various stages of the disease.
Conversely, the novel characterized ERß subtype was
undetectable in human prostate tissue. High-grade prostatic
intraepithelial neoplasia revealed ER mRNA and protein expression in
28% and 11% of cases evaluated. Focal ER immunoreactivity was
detected in a minority of low- to intermediate-grade adenocarcinoma.
High-grade (primary Gleason grade 4 and 5) tumors revealed ER protein
expression in 43% (62% respectively) of cases. The most significant
ER gene expression on mRNA and protein levels was observed in
hormone refractory tumors and metastatic lesions, including
lymph node and bone metastases. Results of the current study suggest
that estrogens can affect prostatic cancerogenesis and neoplastic
progression through an ER-mediated process in human prostate
tissue.
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