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在两只由Tie2启动子驱动Trp53条件性缺失的雌性小鼠中,非妊娠性卵巢绒毛膜癌的免疫组织学描述

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

作者信息

Castiglioni V, Farhang Ghahremani M, Goossens S, De Maglie M, Ardizzone M, Haigh J J, Radaelli E

机构信息

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.

出版信息

Vet Pathol. 2015 Jul;52(4):752-6. doi: 10.1177/0300985814551581. Epub 2014 Sep 24.

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.

摘要

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。

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