Immunohistological Description of Nongestational Ovarian Choriocarcinoma in Two Female Mice With Conditional Loss of Trp53 Driven by the Tie2 Promoter

Author:

Castiglioni V.12,Ghahremani M. Farhang34,Goossens S.345,Maglie M. De12,Ardizzone M.6,Haigh J. J.3,Radaelli E.12

Affiliation:

1. Department of Veterinary Science and Public Health, Veterinary Medicine, University of Milan, Via Celoria, Milan, Italy

2. Mouse & Animal Pathology Lab, Fondazione Filarete, Viale Ortles, Milan, Italy

3. VIB–Department of Molecular Biomedical Research, Vascular Cell Biology Unit, Ghent University, Ghent, Belgium

4. VIB–Molecular Signal Transduction in Inflammation Unit, Inflammation Research Center; VIB–Ghent University, Ghent, Belgium

5. Department for Biomedical Molecular Biology, Ghent University, Ghent, Belgium

6. Merck Serono RBM S.p.A., Istituto di Ricerche Biomediche, Colleretto Giacosa, Italy

Abstract

Nongestational ovarian choriocarcinoma (NGCO) is a tumor of germ cell origin seldom described in nonhuman species. Few spontaneous cases are reported in macaques and mice, with the B6C3F1 strain overrepresented. This report describes 2 cases of ovarian choriocarcinoma in nulliparous female mice with conditional loss of Trp53 under the Tie2 promoter. The mouse line was maintained on a mixed genetic background including Crl: CD1(ICR) and 129X1/SvJ strains. In both cases, affected ovary was partially replaced by blood-filled lacunae lined by neoplastic trophoblast-like giant cells. Immunohistochemically, neoplastic cells expressed folate-binding protein and prolactin and were invariably negative for p53. To the authors’ knowledge, this is the first report characterizing this entity in a genetically engineered mouse (GEM) line. Considering that germ cells (the cell population from which NGCO originates) constitutively express Tie2 receptor, it can be speculated that Tie2-driven deletion of Trp53 may have played a role in the development of these tumors.

Publisher

SAGE Publications

Subject

General Veterinary

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