Home HOME Neoplasma 2009 Neoplasma Vol.56, No.4, p.317-320, 2009

Journal info

6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.56, No.4, p.317-320, 2009

Title: 17β-hydroxysteroid dehydrogenase type 11 (Pan1b) expression in human prostate cancer
Author: Y. Nakamura, T. Suzuki, Y. Arai, H. Sasano

Abstract: Androgens are reported to be actively produced in situ in human prostate cancer. These locally produced androgens are also demonstrated to play important role in the pathogenesis and development of human prostate cancer. The status of locally produced androgen inactivation and metabolism, however, remains unclear. Therefore, it is important to examine the status of this in situ androgen metabolism and inactivation in order to improve clinical response to endocrine therapy in the patients diagnosed with prostate cancer. 17β-hydroxysteroid dehydrogenase type 11 (Pan1b) was demonstrated to display greatest activity with 5α-androstan-3α, 17β-diol (3α-diol) as substrate in several human androgen metabolizing tissues, suggesting that this enzyme may play important role in androgen metabolism. However, its details including the expression level of Pan1b have not been studied in human prostate cancer. In this study, we evaluated immunolocalization of Pan1b in human prostate cancer specimens obtained from surgery (n=40), and correlated the findings with clinicopathological features of the patients in order to study its clinical significance. Pan1b immunoreactivity was detected in 19 cases (48%) and was significantly associated with cancer of seminal vesicle invasion (P

Keywords: 17ß-hydroxysteroid dehydrogenase type XI, prostate cancer, immunochemistry
Year: 2009, Volume: 56, Issue: 4 Page From: 317, Page To: 320

download file

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.