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Insights from mouse models into human retinoblastoma

机译：小鼠模型对人视网膜母细胞瘤的见解

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Novel murine models of retinoblastoma based on Rb gene deletion in concert with inactivation of Rb family members have recently been developed. These new Rb knockout models of retinoblastoma provide excellent tools for pre-clinical studies and for the exploration of the genetics of tumorigenesis driven by RB inactivation. This review focuses on the developmental consequences of Rb deletion in the retina and the genetic interactions between Rb and the two other members of the pocket protein family, p107 (Rbl1) and p130 (Rbl2). There is increasing appreciation that homozygous RB mutations are insufficient for human retinoblastoma. Identifying and understanding secondary gene alterations that cooperate with RB inactivation in tumorigenesis may be facilitated by mouse models. Recent investigation of the p53 pathway in retinoblastoma, and evidence of spatial topology to early murine retinoblastoma are also discussed in this review.
机译：最近已经开发了基于Rb基因缺失和Rb家族成员失活的新型视网膜母细胞瘤小鼠模型。这些新的视网膜母细胞瘤的Rb基因敲除模型为临床前研究和探索由RB失活驱动的肿瘤发生的遗传学提供了极好的工具。这项审查侧重于视网膜上Rb缺失的发展后果以及Rb与口袋蛋白家族的其他两个成员p107（Rbl1）和p130（Rbl2）之间的遗传相互作用。人们越来越认识到纯合的RB突变不足以用于人类视网膜母细胞瘤。小鼠模型可能有助于识别和理解与RB失活在肿瘤发生中协同作用的继发基因改变。本文还讨论了视网膜母细胞瘤中p53途径的最新研究，以及早期鼠视网膜母细胞瘤的空间拓扑学证据。

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