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Mouse models of cervical cancer

机译：子宫颈癌的小鼠模型

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Cervical cancer, a worldwide health problem, has been directly linked to genital infection by human papilloma virus (HPV), and HPV DNA has been detected in nearly all cervical cancers. The HPVs are mucosal-tropic viruses infecting basal squamous epithelial cells, with the productive phase of the viral life cycle elaborated in the upper squamous epithelial cell layers. Most HPV infections are transient, but in a few patients, persistent viral disease develops. This viral persistence is localized inthe basal epithelial cells of the cervix. Persistent viral disease is associated with cervical neoplasia and invasive cervical cancers. Cervical neoplasia and cancer are also linked to infection and persistence of"high-risk" HPV viral types. The HPVs contain two genes in their early region, E6 and E7, and high-risk viral types encode E6 and E7 proteins with enhanced affinity for cellular proteins controlling a collection of functions necessary for neoplastic progression or growth and spread of malignancies. Several studies support a functional role for the E6 and E7 oncogenes in tumorigenesis. Cell transfection of high-risk HPV16 or 18 E6 and E7 oncogenes transforms established cell lines and immortalizes primary cells. Ubiquitous or targeted expression of E6 and E7 has been documented to form benign tumors or cancers in transgenic mice. Expression of the E6 and E7 oncogenes in premalignant dysplastic lesions, and in cervix cancers, is inferential support for a functional role for these viral oncogenes in human carcinogenesis. The potential importance of E6 and E7 function in cervical carcinogenesis has spawned vaccine development targeting viral oncoprotein epitopes. These vaccine efforts are a parallel approach to prophylaxis that is based on immunization against viral capsid antigens. Rational drug design is also being applied to target the enzymatic functions of E6 or more recently E7. Thus, the importance of these HPV oncogenes for viral infection, carcinogenesis, and potential therapy mandatesa complete understanding of their molecular, cellular, and tissue biology in cervical epithelial cells.
机译：宫颈癌是全球性的健康问题，已与人类乳头瘤病毒（HPV）引起的生殖器感染直接相关，并且在几乎所有宫颈癌中均检测到HPV DNA。 HPV是感染基底膜鳞状上皮细胞的黏膜嗜性病毒，其病毒生命周期的生产阶段在上鳞状上皮细胞层中得以阐明。大多数HPV感染是暂时性的，但在少数患者中，会发展为持续性病毒性疾病。这种病毒的持久性位于子宫颈的基底上皮细胞中。持续性病毒疾病与宫颈癌和浸润性宫颈癌有关。宫颈肿瘤和癌症也与“高风险” HPV病毒类型的感染和持续存在有关。 HPV在其早期区域包含两个基因，即E6和E7，高危病毒类型编码E6和E7蛋白，对细胞蛋白的亲和力增强，从而控制了肿瘤发展或恶性肿瘤的生长和扩散所必需的功能集合。多项研究支持E6和E7癌基因在肿瘤发生中的功能性作用。高风险HPV16或18个E6和E7癌基因的细胞转染可转化已建立的细胞系并使永生细胞永生。 E6和E7的普遍表达或靶向表达已被证明在转基因小鼠中形成良性肿瘤或癌症。 E6和E7癌基因在恶性增生前病变和子宫颈癌中的表达为这些病毒癌基因在人类致癌中的功能作用提供了推断支持。 E6和E7功能在宫颈癌变中的潜在重要性催生了针对病毒癌蛋白表位的疫苗开发。这些疫苗工作是基于针对病毒衣壳抗原的免疫预防的并行方法。合理的药物设计也被用于靶向E6或更近期的E7的酶功能。因此，这些HPV癌基因对于病毒感染，致癌作用和潜在治疗的重要性要求对宫颈上皮细胞的分子，细胞和组织生物学有完整的了解。

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