López-Reig Raquel, López-Guerrero José Antonio
Laboratory of Molecular Biology, Fundación Instituto Valenciano de Oncología (IVO), 46009 Valencia, Spain.
IVO-CIPF Joint Research Unit of Cancer, Príncipe Felipe Research Center (CIPF), 46012 Valencia, Spain.
EJC Suppl. 2020 Aug 22;15:27-37. doi: 10.1016/j.ejcsup.2019.12.001. eCollection 2020 Aug.
Epithelial ovarian cancer (EOC) is a heterogeneous group of diseases with distinct biological and clinical behaviour. Despite the differences between them, the capability of tumour cells to continuously proliferate and avoid death is maintained among histotypes. This ability is the result of alterations at different levels, causing the deregulation of cell cycle and proliferative-related pathways. Even if the leading role is played by RB and TP53, changes in other molecular pathways are involved in the development of EOC. This ability can be exploited to generate and models resembling the conditions of tumour development in a patient. models, such as patient-derived xenografts (PDX) or genetically engineered mouse models (GEMM), represent a fundamental tool in the study of the molecular mechanisms implicated in each EOC biotype for testing new therapeutic approaches. Herein we describe the major proliferation-related pathways and its disruption found in EOC and how these features can be used to establish models for translational research.
上皮性卵巢癌(EOC)是一组具有不同生物学和临床行为的异质性疾病。尽管它们之间存在差异,但在不同组织学类型中,肿瘤细胞持续增殖和避免死亡的能力是保持的。这种能力是不同水平改变的结果,导致细胞周期和增殖相关途径的失调。即使RB和TP53起主要作用,但其他分子途径的改变也参与了EOC的发展。这种能力可被用于生成类似于患者肿瘤发展情况的模型。患者来源的异种移植(PDX)或基因工程小鼠模型(GEMM)等模型是研究每种EOC生物型所涉及的分子机制以测试新治疗方法的基本工具。在此,我们描述了在EOC中发现的主要增殖相关途径及其破坏情况,以及如何利用这些特征建立用于转化研究的模型。