scholarly journals Ageing, testicular tumours and the pituitary-testis axis in dogs

2000 ◽  
Vol 166 (1) ◽  
pp. 153-161 ◽  
Author(s):  
MA Peters ◽  
FH de Jong ◽  
KJ Teerds ◽  
DG de Rooij ◽  
SJ Dieleman ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Venous Blood ◽  
Cell Tumour ◽  
Age Related ◽  
Sertoli Cell Tumour ◽  
Leydig Cell Tumour ◽  
Sertoli Cell Tumours ◽  
Leydig Cell Tumours ◽  
Age Related Changes

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.

NEW VIEWS ON THE HORMONE-PRODUCING MESENCHYMOMAS OF THE OVARIES

1960 ◽  
Vol XXXV (IV) ◽  
pp. 513-517
Author(s):  
W. P. Plate
Keyword(s):  
Granulosa Cell ◽  
Sertoli Cell ◽  
Leydig Cell ◽  
Cell Tumour ◽  
Theca Cell ◽  
Granulosa Cell Tumour ◽  
Sertoli Cell Tumours ◽  
Leydig Cell Tumours

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.

Testicular Sertoli cell tumour and potentially testicular Leydig cell tumour are features of DICER1 syndrome

2021 ◽  
pp. jmedgenet-2020-107434
Author(s):  
Lisa Golmard ◽  
Lauren M Vasta ◽  
Valérie Duflos ◽  
Carole Corsini ◽  
Catherine Dubois d'Enghien ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Autosomal Dominant ◽  
Pathogenic Variant ◽  
Cell Tumour ◽  
Malignant Tumours ◽  
Tumour Diagnosis ◽  
Sertoli Cell Tumour ◽  
Leydig Cell Tumour ◽  
Dicer1 Syndrome

DICER1 syndrome is a rare paediatric autosomal dominant inherited disorder predisposing to various benign and malignant tumours. It is caused by a germline pathogenic variant in DICER1, and the second hit for tumour development is usually a missense hotspot pathogenic variant in the DICER1 ribonuclease IIIb domain. While DICER1 predisposing variants account for about 60% of ovarian Sertoli-Leydig cell tumours, no DICER1-related testicular stromal tumours have been described. Here we report the first two cases of testicular stromal tumours in children carrying a DICER1 germline pathogenic variant: a case of Sertoli cell tumour and a case of Leydig cell tumour diagnosed at 2 and 12 years of age, respectively. A somatic DICER1 hotspot pathogenic variant was detected in the Sertoli cell tumour. This report extends the spectrum of DICER1-related tumours to include testicular Sertoli cell tumour and potentially testicular Leydig cell tumour. Diagnosis of a testicular Sertoli cell tumour should prompt DICER1 genetic testing so that patients with a DICER1 germline pathogenic variant can benefit from established surveillance guidelines. DICER1 genetic evaluation may be considered for testicular Leydig cell tumour. Our findings suggest that miRNA dysregulation underlies the aetiology of some testicular stromal tumours.

Mixed Testicular Neoplasia in a Common Dolphin (Delphinus delphis) Involving Sertoli Cell Tumour, Interstitial (Leydig) Cell Tumour and Seminoma

2013 ◽  
Vol 148 (1) ◽  
pp. 91
Author(s):  
M. Arbelo ◽  
J. Díaz-Delgado ◽  
A. Espinosa de los Monteros ◽  
C. Fernández-Maldonado ◽  
O. Quesada ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Cell Tumour ◽  
Common Dolphin ◽  
Delphinus Delphis ◽  
Sertoli Cell Tumour ◽  
Leydig Cell Tumour

Spermatogenesis and testicular tumours in ageing dogs

Reproduction ◽  
2000 ◽  
pp. 443-452 ◽  
Author(s):  
MA Peters ◽  
DG de Rooij ◽  
KJ Teerds ◽  
I van Der Gaag ◽  
FJ van Sluijs
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Seminiferous Tubules ◽  
Score System ◽  
Testicular Tumours ◽  
Severe Impairment ◽  
Per Se ◽  
Testicular Disease ◽  
Sertoli Cell Tumours ◽  
Leydig Cell Tumours

Spermatogenesis was examined in testes from 74 dogs of various breeds without clinically detected testicular disease. A modified Johnsen score system was used to determine whether spermatogenesis deteriorates with ageing. The diameter of seminiferous tubules was measured in dogs without testicular disease to examine other possible effects of ageing on tubular performance. There appeared to be no relation between age and these variables. The influence of testicular tumours on spermatogenesis was also investigated in both affected and unaffected testes. The testes of 28 dogs with clinically palpable tumours and 21 dogs with clinically non-palpable tumours were investigated. In cases of unilateral occurrence of a tumour, impairment of spermatogenesis was observed only in the affected testis of dogs with clinically detected tumours. Bilateral occurrence of tumours, whether detected clinically or non-clinically, was associated with severe impairment of spermatogenesis. The prevalence of tumours increased during ageing. Eighty-six per cent of the clinically detected and 57% of the non-clinically detected tumours were found in old dogs. Multiple types of tumour and bilateral occurrence were very common. Seminomas and Leydig cell tumours were more frequent than Sertoli cell tumours. It was concluded that spermatogenesis per se did not decrease during ageing in dogs but the occurrence of testicular tumours increased with ageing and affected spermatogenesis significantly, as reflected by a lower Johnsen score.

scholarly journals Expression of Selected Markers in Immunohistochemical Diagnosis of Canine and Human Testicular Tumours

2015 ◽  
Vol 59 (1) ◽  
pp. 99-106
Author(s):  
Rafał Ciaputa ◽  
Marcin Nowak ◽  
Janusz A. Madej ◽  
Izabela Janus ◽  
Elżbieta Górzyńska ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Von Willebrand Factor ◽  
Leydig Cell ◽  
Chromogranin A ◽  
Testicular Tumours ◽  
Immunohistochemical Diagnosis ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Sertoli Cell Tumours ◽  
Leydig Cell Tumours

Abstract Immunohistochemical profiles of the most common canine testicular tumours, including the Leydig cell tumours, seminomas, and Sertoli cell tumours were analysed, and the results were compared with those obtained in the corresponding types of human testicular neoplasms. The expressions of vimentin, von Willebrand factor (FVIII), chromogranin A, synaptophysin, and MCM3 were quantified. In the case of Sertoli cell tumours, only canine ones were analysed, since this type of tumour is very rarely diagnosed in men. The expression of the analysed proteins in the testicular tumours was similar. The von Willebrand factor exhibited the strongest expression in Leydig cell tumours in dogs and men, while vimentin was expressed more strongly in dogs (96.7% had an intensity at +++) than in men (62.5% had +++) in the Leydigioma. The immunoexpression of MCM3 in seminomas was high in both men and dogs – 90% +++ and 100% +++ respectively. The lack of chromogranin A and synaptophysin was observed in almost 100% of seminomas in men and dogs. This differed from the results obtained for Leydigioma, where chromogranin A was expressed in 70% of dogs at +++ and in 100% of men at ++++. The results may indicate that the antibodies were selected correctly. Their analysis and interpretation provides valuable information concerning the nature of the studied tumours.

scholarly journals Use of antibodies against LH receptor, 3beta-hydroxysteroid dehydrogenase and vimentin to characterize different types of testicular tumour in dogs

Reproduction ◽  
2001 ◽  
pp. 287-296 ◽  
Author(s):  
MA Peters ◽  
KJ Teerds ◽  
I van der Gaag ◽  
DG de Rooij ◽  
FJ van Sluijs
Keyword(s):  
Sertoli Cell ◽  
Leydig Cell ◽  
Leydig Cells ◽  
Hydroxysteroid Dehydrogenase ◽  
Histological Diagnosis ◽  
Lh Receptor ◽  
Testicular Tumours ◽  
Sertoli Cell Tumours ◽  
Mixed Tumours ◽  
Leydig Cell Tumours

Testicular tumours in dogs are of Sertoli cell, Leydig cell or germinal origin and mixed tumours are also frequently observed. The cellular components of mixed tumours are usually identified by histological examination but sometimes this is difficult. In this study, a panel of specific antibodies was used to identify the different cell types in testicular tumours by immunohistochemistry. Leydig cells were identified using an antibody against the LH receptor and an antibody against the steroidogenic enzyme 3beta-hydroxysteroid dehydrogenase (3beta-HSD), both of which are characteristic of Leydig cells in testes. Sertoli cells were identified using an antibody against the intermediate filament vimentin. Seminoma cells did not stain with any of these antibodies. Vimentin was used only in histologically complex cases. Eighty-six tumours, diagnosed histologically as 29 Sertoli cell tumours, 25 Leydig cell tumours, 19 seminomas and 13 mixed tumours, were studied. Feminization was observed in 17 dogs. Leydig cell tumours stained positively with the antibodies against the LH receptor and 3beta-HSD, whereas seminomas and Sertoli cell tumours were negative (unstained). The antibody against vimentin stained both Sertoli and Leydig cells, and tumours arising from these cells, but not seminomas. Immunohistochemistry revealed that three tumours identified histologically as Sertoli cell tumours were actually Leydig cell tumours. In 14 dogs the histological diagnosis appeared to be incomplete, as mixed tumours instead of pure types of tumours were identified in 11 dogs, and in three dogs mixed tumours appeared to be pure types. Hence, the histological diagnosis was insufficient in approximately 20% of dogs. Furthermore, immunohistochemical analysis of testis tumours revealed that feminization occurred in dogs with Sertoli cell tumours or Leydig cell tumours and their combinations, but not in dogs with a seminoma. In conclusion, incubation with antibodies against LH receptor and 3beta-HSD proved to be a consistently reliable method for identification of Leydig cell tumours in dogs. Vimentin can be used to discriminate between Sertoli cell tumours and seminomas. Overall, this panel of antibodies can be very useful for determination of the identity of testicular tumours in which histological characterization is complicated and the pathogenesis of feminization is not clear.

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 ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Sertoli Cells ◽  
Tumour Progression ◽  
Cell Development ◽  
Cell Tumour ◽  
Wild Type ◽  
Sertoli Cell Tumour ◽  
Dynamic Partnership ◽  
Sertoli Cell Tumours ◽  
Developmental Windows

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.

scholarly journals A Unique Case of a Malignant Sertoli Cell Tumour with Cutaneous Metastasis

2008 ◽  
Vol 8 ◽  
pp. 95-97 ◽  
Author(s):  
C. Blick ◽  
S. Abdelhadi ◽  
D. Bailey ◽  
J. Kelleher ◽  
A. Muneer
Keyword(s):  
Sertoli Cell ◽  
Primary Tumour ◽  
Cutaneous Lesion ◽  
Cutaneous Metastasis ◽  
Testicular Neoplasms ◽  
Cell Tumour ◽  
Unique Case ◽  
First Case ◽  
Sertoli Cell Tumour ◽  
Sertoli Cell Tumours

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.

scholarly journals Malignant Leydig cell tumour in a Tupaia belangeri: case report and literature review of male genital tumours in non-human primates

1988 ◽  
Vol 22 (2) ◽  
pp. 131-134 ◽  
Author(s):  
M. Brack
Keyword(s):  
Leydig Cell ◽  
Cell Tumour ◽  
Genital System ◽  
Tupaia Belangeri ◽  
Short Summary ◽  
Male Genital System ◽  
Leydig Cell Tumour ◽  
Haematogenous Spread ◽  
Sertoli Cell Tumours ◽  
Male Genital

After a short summary of the few reported tumours of the male genital system in non-human primates, a malignant Leydig cell tumour is described in an adult male Tupaia belangeri. The tumour had metastasized in the omentum probably by haematogenous spread enabled by the peculiar perivascular growth pattern of the tumour cells. Its differential diagnosis versus seminomas and Sertoli cell tumours is discussed.

Hyperandrogenism caused by ovarian Leydig cell tumour: finding the needle in a haystack

2020 ◽  
Vol 13 (12) ◽  
pp. e238012
Author(s):  
Chin Voon Tong ◽  
Yong Ting Tai
Keyword(s):  
Leydig Cell ◽  
Specific Treatment ◽  
Cell Tumour ◽  
Imaging Modalities ◽  
Surgical Removal ◽  
Venous Sampling ◽  
Ovarian Tumours ◽  
Potentially Malignant ◽  
Leydig Cell Tumour ◽  
Leydig Cell Tumours

Leydig cell tumours (LCTs) of the ovary are rare ovarian tumours that usually present with hyperandrogenism. Conventional radiological imagings are helpful in localising these tumours. However, some tumours may be too small to be localised before curative surgical removal. It is important to identify these androgen-secreting neoplasms which originate mostly from adrenals or ovaries because they are potentially malignant and require specific treatment. When conventional imagings are unrevealing, selective ovarian and adrenal venous sampling (SOAVS) is the next option. We report a case of LCT that was localised by SOAVS after results from other imaging modalities remained inconclusive.

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