Eur J Endocrinol
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DOI: 10.1530/EJE-07-0029
European Journal of Endocrinology, Vol 157, Issue 2, 239-244
Copyright © 2007 by European Society of Endocrinology
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CASE REPORT

Detection of aromatase and estrogen receptors (ER{alpha}, ERß1, ERß2) in human Leydig cell tumor

Amalia Carpino, Vittoria Rago, Vincenzo Pezzi1, Cesare Carani2 and Sebastiano Andò

Departments of Cell Biology and 1 Pharmaco-Biology, Faculty of Pharmacy, University of Calabria, 87030 Arcavacata di Rende (CS), Italy and 2 Department of Internal Medicine, University of Modena and Reggio Emilia, Policlinico, 411000 Modena, Italy

(Correspondence should be addressed to S Andò who is now at Dipartimento di Biologia Cellulare, Università degli Studi della Calabria, Arcavacata di Rende, 87030 Cosenza, Italy; Email: sebastiano.ando{at}unical.it)

Abstract

A Leydig cell tumor is a rare neoplasm, deriving from the interstitial cells, whose pathogenesis has not been still defined. Leydig cells of normal adult testis are known as physiological targets for estrogens. However, some studies on transgenic rodents suggest a role of estrogens in the development of Leydig cell hyperplasia and Leydig cell tumor. Therefore, with the aim to evaluate a possible link between estrogens and testicular tumorigenesis, this study investigated the expression of aromatase and estrogen receptors (ER{alpha}, ERß1, ERß2) in testes from two patients with Leydig cell tumor. A strong immunoreactivity for aromatase, ERß1, and ERß2, together with a detectable ER{alpha} immunostaining, was revealed in tumoral tissues. These findings were confirmed by western blot analysis of tumor extracts detecting a 55 kDa P450arom, a 67 kDa ER{alpha} band, a 59 kDa ERß1 band, and a 53 kDa ERß2 band. The pattern of ER expression in neoplastic cells appears different from that of control Leydig cells exhibiting only ERß1 and ERß2 isoforms. The authors hypothesize how the high estrogen production could play a role in the neoplastic transformation of Leydig cells, while the exclusive presence of ER{alpha} in tumoral cells could amplify estradiol-17ß signaling contributing to the tumor cell growth and progression.







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Copyright © 2007 European Society of Endocrinology.