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Genetic risk factors in tumours of the testis: lessons from twin studies

Published online by Cambridge University Press:  21 February 2012

Cornelis B Lambalk*
Affiliation:
Division of Reproductive Endocrinology, Research Institute for Endocrinology, Reproduction and Metabolism, Department of Obstetrics/Gynaecology, Academic Hospital, Free University, Amsterdam. cb.lambalk@azvu.nl
Dorret I Boomsma
Affiliation:
Department of Psychonomics, Faculty of Psychology, Free University, Amsterdam, The Netherlands.
*
*Correspondence: Dr Cornelis B Lambalk, Division of Reproductive Endocrinology, Research Institute for Endocrinology, Reproduction and Metabolism, Department of Obstetrics/Gynaecology, Academic Hospital, Free University, PO Box 7057, 1007 MB Amsterdam, The Netherlands. Tel: 00 31 20 444 0070; Fax: 00 31 20 444 0045

Abstract

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A threefold increase for testicular carcinoma has been reported in male dizygotic twins. In this comment we suggest the hypothesis that over-exposure to endogenously hypersecreted Follicle Stimulating Hormone (FSH) may underlie the pathogenesis. This is supported by several findings. 1) FSH hypersecretion in mothers of dizygotic twins is most likely an autosomal trait implicating the possibility of male offspring with the same hormone characteristic. 2) In testicular carcinoma higher levels of cyclin D2 are found. This is an FSH dependent stimulatory regulator of mitosis. 3) There is a marked similarity between geographical distribution in occurence of dizygotic twinning and testicular carcinoma. 4) Men undergoing surgery for testicular carcinoma have higher FSH concentrations and males with Down syndrome have higher FSH levels and are more at risk to develop testicular carcinoma. We suggest to study FSH secretion in males of familial dizygotic twins and furthermore the risk of developing testicular carcinoma in males with elevated FSH. These men with one testicle and/or with dysfunctioning Sertoli/Leydig cells.

Type
Articles
Copyright
Copyright © Cambridge University Press 1998