Human papillomavirus and cervical carcinogenesis
Human papillomavirus and cervical carcinogenesis
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DOI：
10.1053/beog.2001.0213
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发表时间：
2001-10-01
影响因子：
5.5
通讯作者：
Stanley, MA
中科院分区：
文献类型：
--
作者：
Stanley, MA
流行病学研究表明，生殖器人类乳头瘤病毒（HPV）感染是随后发展为宫颈癌的主要危险因素。实验研究表明，这些高危hpv的E6和E7基因是解除关键细胞周期控制的致癌基因。在正常的感染周期中，这些基因的高水平表达仅限于未分裂的分化细胞：HPV的发生需要解除病毒和细胞基因的管制，从而允许E6和E7的不适当表达。这些都是罕见的事件，但病毒的持久性和长期暴露于类固醇激素增加了这种解除管制的可能性。
Epidemiological studies show that infection with a subset of genital human papillomavirus (HPV) infections is the major risk factor for the subsequent development of cervical cancer. Experimental studies show that that the E6 and E7 genes of these high risk HPVs are oncogenes that deregulate key cell cycle controls. In the normal infectious cycle high level expression of these genes is confined to non-dividing differentiated cells: HPV oncogenesis requires deregulation of viral and cellular genes permitting inappropriate expression of E6 and E7. These are rare events but viral persistence and chronic exposure to steroid hormones increase the probability of this deregulation.