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Characteristics of in Vivo Model Systems for Ovarian Cancer Studies.
Tudrej P, Kujawa KA, Cortez AJ, Lisowska KM.
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An understanding of the molecular pathogenesis and heterogeneity of ovarian cancer holds promise for the development of early detection strategies and novel, efficient therapies. In this review, we discuss the advantages and limitations of animal models available for basic and preclinical studies. The fruit fly model is suitable mainly for basic research on cellular migration, invasiveness, adhesion, and the epithelial-to-mesenchymal transition. Higher-animal models allow to recapitulate the architecture and microenvironment of the tumor. We discuss a syngeneic mice model and the patient derived xenograft model (PDX), both useful for preclinical studies. Conditional knock-in and knock-out methodology allows to manipulate selected genes at a given time and in a certain tissue. Such models have built our knowledge about tumor-initiating genetic events and cell-of-origin of ovarian cancers; it has been shown that high-grade serous ovarian cancer may be initiated in both the ovarian surface and tubal epithelium. It is postulated that clawed frog models could be developed, enabling studies on tumor immunity and anticancer immune response. In laying hen, ovarian cancer develops spontaneously, which provides the opportunity to study the genetic, biochemical, and environmental risk factors, as well as tumor initiation, progression, and histological origin; this model can also be used for drug testing. The chick embryo chorioallantoic membrane is another attractive model and allows the study of drug response.
Figure 1.
(A) Schematic diagram of reproductive system of Drosophila melanogaster. (B) Migration of border cells in the developing ovarian follicle. GSC—germline stem cell, FSC—follicle stem cell, aPC—anterior polar cell, pPC—posterior polar cell, BC—border cell, FC—follicle cell, NC—nurse cell.
Figure 2.
Mouse model designed by Orsulic et al. [67] to evaluate oncogenes necessary for neoplastic transformation of ovarian surface epithelium (OSE) cells with an inactive p53 gene. TVA, tumor virus receptor A.
Figure 3.
Mouse model used by Flesken-Nikitin et al. [71] for specific knock-out of p53 and pRb genes in OSE cells.
Figure 4.
Mouse model used by Perets et al. [73] for the tissue-specific knock-out of the p53 and Brca1 genes, using Cre recombinase, the expression of which was limited to the Müllerian epithelia and induced after administration of the tetracycline.
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