Document Detail


Origin and evolution of somatic cell testicular tumours in transgenic mice.
MedLine Citation:
PMID:  20593483     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Transgenic mice bearing a construct in which the expression of the SV40 oncogene is directed by the AMH promoter (AT mice) develop testicular tumours in adult life. We aimed to study early steps of tumour development and characterize tumours at different ages by histological, morphometric, and immunohistochemical techniques. One- to 3-month-old AT mice depicted multifocal Leydig cell hyperplasia. The testicular volume occupied by interstitial tissue was significantly higher in 3-month-old AT mice in comparison with littermate controls. Between 5 1/2 and 7 months, microscopic interstitial tumours developed that progressively evolved to form large confluent areas of high mitotic index in 7- to 14-month-old AT mice. Tumour cells had the characteristics and histoarchitecture of Leydig cells, or formed solid cord-like structures reminiscent of those seen in Sertoli cell tumours. Hyperplastic areas and tumours diffusely expressed 3beta-hydroxysteroid dehydrogenase (3beta-HSD) in Leydig cell areas. AMH expression was negative in Leydig cell conglomerates and tumours and variable in cord-like tumours. The SV40 T antigen and markers of cell proliferation (PCNA) were intensely positive in hyperplastic cells and tumours. Control mice of similar ages showed neither hyperplasia nor tumours, and SV40 T expression was always negative. In conclusion, transgenic mice develop large testicular tumours that are preceded by interstitial hyperplasia and microtumours. The histological and immunohistochemical phenotype of tumours (Leydig and Sertoli cell differentiation, positive 3beta-HSD, and variable AMH) suggests a mixed differentiation of somatic cells of the specialized gonadal stroma. The finding that an oncogene directed by a promoter specifically active in fetal Sertoli cells has given rise to testicular tumours of mixed differentiation is compatible with a common origin of Leydig and Sertoli cells from the specific stroma of the gonadal ridge, as supported by double labelling experiments in fetal mice showing co-localization of the transgene with Sertoli and Leydig cell markers.
Authors:
Silvina Quintana; Marcela Venara; Rodolfo Rey; Nathalie di Clemente; Héctor E Chemes
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of pathology     Volume:  221     ISSN:  1096-9896     ISO Abbreviation:  J. Pathol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-07     Completed Date:  2010-08-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0204634     Medline TA:  J Pathol     Country:  England    
Other Details:
Languages:  eng     Pagination:  443-51     Citation Subset:  IM    
Affiliation:
Center for Research in Endocrinology (CEDIE-CONICET), Buenos Aires Children's Hospital, Gallo 1330, Buenos Aires, Argentina.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Polyomavirus Transforming / metabolism
Cell Differentiation
Cell Transformation, Neoplastic / metabolism,  pathology
Hyperplasia / pathology
Leydig Cell Tumor / metabolism,  pathology*
Leydig Cells / pathology
Male
Mice
Mice, Transgenic
Sertoli Cells / pathology
Testicular Neoplasms / metabolism,  pathology*
Chemical
Reg. No./Substance:
0/Antigens, Polyomavirus Transforming

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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