Castiglioni V, Farhang Ghahremani M, Goossens S, De Maglie M, Ardizzone M, Haigh J J, Radaelli E
Department of Veterinary Science and Public Health, Veterinary Medicine, University of Milan, Via Celoria, Milan, Italy Mouse & Animal Pathology Lab, Fondazione Filarete, Viale Ortles, Milan, Italy
VIB-Department of Molecular Biomedical Research, Vascular Cell Biology Unit, Ghent University, Ghent, Belgium VIB-Molecular Signal Transduction in Inflammation Unit, Inflammation Research Center; VIB-Ghent University, Ghent, Belgium.
Vet Pathol. 2015 Jul;52(4):752-6. doi: 10.1177/0300985814551581. Epub 2014 Sep 24.
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.
非妊娠性卵巢绒毛膜癌（NGCO）是一种起源于生殖细胞的肿瘤，在非人类物种中很少被描述。在猕猴和小鼠中报告的自发病例很少，其中B6C3F1品系的病例占比过高。本报告描述了2例在Tie2启动子下Trp53条件性缺失的未生育雌性小鼠发生卵巢绒毛膜癌的病例。该小鼠品系维持在包括Crl:CD1(ICR)和129X1/SvJ品系的混合遗传背景上。在这两个病例中，受影响的卵巢部分被充满血液的腔隙所取代，腔隙内衬有肿瘤性滋养层样巨细胞。免疫组织化学显示，肿瘤细胞表达叶酸结合蛋白和催乳素，p53始终为阴性。据作者所知，这是首次在基因工程小鼠（GEM）品系中对该实体进行特征描述。鉴于生殖细胞（NGCO起源的细胞群体）组成性表达Tie2受体，可以推测Tie2驱动的Trp53缺失可能在这些肿瘤的发生中起了作用。
