scholarly journals Suppression of Sertoli cell tumour development during the first wave of spermatogenesis in inhibin α-deficient mice

2017 ◽  
Vol 29 (3) ◽  
pp. 609 ◽  
Author(s):  
Jenna T. Haverfield ◽  
Peter G. Stanton ◽  
Kate L. Loveland ◽  
Heba Zahid ◽  
Peter K. Nicholls ◽  
...  

A dynamic partnership between follicle-stimulating hormone (FSH) and activin is required for normal Sertoli cell development and fertility. Disruptions to this partnership trigger Sertoli cells to deviate from their normal developmental pathway, as observed in inhibin α-knockout (Inha-KO) mice, which feature Sertoli cell tumours in adulthood. Here, we identified the developmental windows by which adult Sertoli cell tumourigenesis is most FSH sensitive. FSH was suppressed for 7 days in Inha-KO mice and wild-type littermates during the 1st, 2nd or 4th week after birth and culled in the 5th week to assess the effect on adult Sertoli cell development. Tumour growth was profoundly reduced in adult Inha-KO mice in response to FSH suppression during Weeks 1 and 2, but not Week 4. Proliferative Sertoli cells were markedly reduced in adult Inha-KO mice following FSH suppression during Weeks 1, 2 or 4, resulting in levels similar to those in wild-type mice, with greatest effect observed at the 2 week time point. Apoptotic Sertoli cells increased in adult Inha-KO mice after FSH suppression during Week 4. In conclusion, acute FSH suppression during the 1st or 2nd week after birth in Inha-KO mice profoundly suppresses Sertoli cell tumour progression, probably by inhibiting proliferation in the adult, with early postnatal Sertoli cells being most sensitive to FSH action.

2008 ◽  
Vol 8 ◽  
pp. 95-97 ◽  
Author(s):  
C. Blick ◽  
S. Abdelhadi ◽  
D. Bailey ◽  
J. Kelleher ◽  
A. Muneer

Pure Sertoli cell tumours (SCTs) represent less than 1% of testicular neoplasms and malignant forms are rare. We present a unique case of a 69-year-old man who initially underwent inguinal orchidectomy for a malignant SCT. He then subsequently developed a paraumbilical cutaneous lesion which was histologically identical to the primary tumour. SCTs rarely metastasise. This is the first case of SCT with cutaneous metastasis described in the literature.


2009 ◽  
Vol 296 (5) ◽  
pp. E1022-E1028 ◽  
Author(s):  
Charles M. Allan ◽  
Patrick Lim ◽  
Mathew Robson ◽  
Jenny Spaliviero ◽  
David J. Handelsman

We have characterized the in vivo actions of human wild-type FSH receptor (FSHR) overexpressed in Sertoli cells of transgenic (Tg) mice ( TgFSHRwt) compared with transgenic overexpression of the human activated mutant FSHR*D567G ( TgFSHR*D567G). Testicular TgFSHRwt expression significantly elevated specific FSH binding (>2-fold, P < 0.01) relative to nontransgenic testes, similar to increased FSH binding in TgFSHR*D567G testes. Isolated TgFSHRwt Sertoli cells exhibited higher FSH-stimulated cAMP levels compared with non- Tg or TgFSHR*D567G cells but did not display the elevated FSH-independent basal cAMP levels found in TgFSHR*D567G Sertoli cells. Furthermore, Sertoli cell overexpression of TgFSHR*D567G but not TgFSHRwt allowed promiscuous cAMP responses to human chorionic gonadotropin (300 IU/ml) and TSH (30 mIU/ml), demonstrating increased constitutive signaling and altered glycoprotein hormone specificity via the intracellular D567G substitution rather than FSHR overexpression. Despite elevating Sertoli cell FSH sensitivity, overexpression of TgFSHRwt had no detectable effect upon normal testis function and did not stimulate Sertoli and germ cell development in testes of gonadotropin-deficient hypogonadal ( hpg) mice, in contrast to the increased meiotic and postmeiotic germ cell development in TgFSHR*D567G hpg testes. Increased steroidogenic potential of TgFSHR*D567G hpg testes was demonstrated by elevated Cyp11a1 and Star expression, which was not detected in TgFSHRwt hpg testes. Androgen-regulated and Sertoli cell-specific Rhox5 gene expression was increased in TgFSHR*D567G but not TgFSHRwt hpg testes, providing evidence of elevated LH-independent androgen activity due to mutant FSHR*D567G. Hence, transgenic FSHR overexpression in Sertoli cells revealed that the D567G mutation confers autonomous signaling and steroidogenic activity in vivo as well as promiscuous glycoprotein hormone receptor activation, independently of FSHR overexpression alone.


1956 ◽  
Vol 14 (2) ◽  
pp. 197-203 ◽  
Author(s):  
W. G. SILLER

SUMMARY The appearance of a spontaneous Sertoli cell tumour in a Brown Leghorn capon has been described. The plumage pattern abnormalities of this bird were shown to be due to a prolonged secretion of oestrogen and may be interpreted as evidence of feminization. This is further proof that Sertoli cells secrete oestrogen.


2000 ◽  
Vol 166 (1) ◽  
pp. 153-161 ◽  
Author(s):  
MA Peters ◽  
FH de Jong ◽  
KJ Teerds ◽  
DG de Rooij ◽  
SJ Dieleman ◽  
...  

Dogs of different ages without testicular diseases were evaluated to study possible age-related changes in hormone concentrations in serum. Dogs with testicular tumours were also investigated to study the relation between tumour type and hormone concentrations; in this study, dogs with Sertoli cell tumours, Leydig cell tumours and seminomas were included. We measured testosterone, oestradiol, LH, FSH and inhibin-like immunoreactivity concentrations in peripheral venous and testicular venous blood of these animals. In normal dogs there appeared to be no age-related changes in the concentrations of the investigated hormones, except for a significant age-related decrease in oestradiol concentrations in testicular venous blood (P<0.02). Dogs with a Sertoli cell tumour had greater oestradiol concentrations and inhibin-like immunoreactivity in both peripheral and testicular venous blood than did dogs without a neoplasm (P<0. 05). Testosterone concentrations were reduced in dogs with Sertoli cell tumours, as were FSH and LH. Feminisation occurred in eight of 13 dogs with a Sertoli cell tumour and in two of 14 dogs with a Leydig cell tumour; it was accompanied by a significantly greater oestradiol concentration than in normal dogs and in dogs with Sertoli cell tumours without signs of feminisation. Dogs with a Leydig cell tumour had greater concentrations of oestradiol and inhibin-like immunoreactivity in both peripheral venous and testicular venous blood than did dogs without a neoplasm (P<0.05). The testosterone concentration in testicular venous blood of these dogs was lower than that in dogs with normal testes. The concentration of LH in peripheral venous blood was also reduced (P<0. 05). Hormone concentrations in dogs with a seminoma were not different from those in normal dogs. It was concluded that seminomas are not endocrinologically active. In contrast, both Sertoli cell tumours and Leydig cell tumours can cause increased oestrogen production leading to signs of feminisation. These tumours also have considerable amounts of inhibin-like immunoreactivity, but only in Sertoli cell tumours does this result in a reduction in FSH concentrations, suggesting that Sertoli cell tumours secrete dimeric inhibin, whereas Leydig cell tumours presumably produce loose alpha-subunits that cross-react in the inhibin assay but are not biologically active.


1960 ◽  
Vol XXXV (IV) ◽  
pp. 513-517
Author(s):  
W. P. Plate

ABSTRACT The hormone-producing mesenchymomas of the ovaries can be divided into androblastomas and gynaecoblastomas. The former are derived from »male« elements, and consist of Sertoli-cell tumours and Leydig-cell tumours. The latter arise from »female« elements and consist of granulosacell tumours and theca-cell tumours. Sertoli-cell tumours and granulosacell tumours produce oestrogens, while Leydig-cell tumours and theca-cell tumours produce oestrogens or androgens. Histologically, androblastomas and gynaecoblastomas are often difficult to distinguish. Since no »female« elements occur in a testicle, a granulosa-cell tumour in a testicle is improbable. Gynandroblastomas, therefore, can only be found in an ovary.


2006 ◽  
Vol 166 (10) ◽  
pp. 1083-1085 ◽  
Author(s):  
Guy Massa ◽  
Nele Roggen ◽  
Marleen Renard ◽  
Johan J. P. Gille

2006 ◽  
Vol 9 (2) ◽  
pp. 18-21
Author(s):  
Sia SF ◽  
Dublin N ◽  
Nurul B ◽  
Wong KT

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