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Differential Gene Expression of Steroid 5α-Reductase 2 in Core Needle Biopsies from Malignant and Benign Prostatic Tissue1

Androgens are implicated in the development of prostate cancer (CAP) and benign prostate hyperplasia. The conversion of testosterone to the more potent metabolite dihydrotestosterone by prostate-specific steroid 5α-reductase type 2 (5α-red2) is a key mechanism in the action of androgens in the prost...

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Bibliographic Details
Published in:The journal of clinical endocrinology and metabolism 1997-07, Vol.82 (7), p.2210-2214
Main Authors: Bjelfman, Catarina, Söderström, Torbjörn G, Brekkan, Einar, Norlén, Bo Johan, Egevad, Lars, Unge, Torsten, Andersson, Stefan, Rane, Anders
Format: Article
Language:English
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Summary:Androgens are implicated in the development of prostate cancer (CAP) and benign prostate hyperplasia. The conversion of testosterone to the more potent metabolite dihydrotestosterone by prostate-specific steroid 5α-reductase type 2 (5α-red2) is a key mechanism in the action of androgens in the prostate and is important in the promotion and progression of prostate diseases. Manipulation of the turnover of androgens is thus fundamental in the pharmacological treatment strategy. We have developed a sensitive solution hybridization method for quantification of the gene expression of 5α-red2 in core needle biopsies of the prostate. The 5α-red2-specific messenger RNA (mRNA) levels were measured in 50 human prostate transrectal ultrasound-guided core biopsies obtained from 31 outpatients (median age 72, range 57–88 yr) undergoing biopsy for diagnostic purposes. Significant differences were observed in the gene expression of 5α-red2 between cancerous and noncancerous tissue. In the 14 biopsies judged cancerous, the median 5α-red mRNA levels were 3.5 amol/ng total RNA compared with 12.0 amol/ng total RNA in the biopsies showing no cancer (P = 0.0018). The median 5α-red2 mRNA level in noncancerous tissue was thus 3.4 times higher than in the cancerous specimens.
ISSN:0021-972X
1945-7197
DOI:10.1210/jcem.82.7.4080