卵巢癌小鼠模型：当前模型及其局限性综述。
Ovarian cancer mouse models: a summary of current models and their limitations.
机构信息
Department of Physiology and Biophysics, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202, USA.
出版信息
J Ovarian Res. 2009 Sep 28;2(1):12. doi: 10.1186/1757-2215-2-12.
Abstract
Development of mouse models representing human spontaneous ovarian cancer has been hampered by the lack of understanding of the etiology of this very complex disease. Mouse models representing the different types of ovarian cancer are needed to understand how epithelial ovarian cancer differs from granulosa cell tumors. Many different methods have been used to generate a viable genetic model with limited success. This review focuses on the methods of various investigators and the limitations of each model in establishing a reproducible and inheritable line to study this disease.
摘要
开发代表人类自发性卵巢癌的小鼠模型一直受到阻碍，因为人们对这种非常复杂疾病的病因缺乏了解。需要开发代表不同类型卵巢癌的小鼠模型，以了解上皮性卵巢癌与颗粒细胞瘤的区别。已经使用了许多不同的方法来生成可行的遗传模型，但收效甚微。这篇综述重点介绍了各个研究人员的方法以及每个模型在建立可重现和可遗传的系以研究这种疾病方面的局限性。
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Expression of activated PIK3CA in ovarian surface epithelium results in hyperplasia but not tumor formation.卵巢表面上皮中活化的PIK3CA的表达导致增生，但不会形成肿瘤。
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Synergistic effects of Pten loss and WNT/CTNNB1 signaling pathway activation in ovarian granulosa cell tumor development and progression.Pten缺失与WNT/CTNNB1信号通路激活在卵巢颗粒细胞瘤发生发展中的协同作用。
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