阻断 HPV 诱导损伤发展的分子机制及潜在靶点。
Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development.
机构信息
Division of Chronic Infections and Cancer, Research Center for Infectious Diseases, Instituto Nacional de Salud Pública, Avenida Universidad No. 655, Cuernavaca 62100, Morelos, Mexico.
出版信息
J Oncol. 2012;2012:278312. doi: 10.1155/2012/278312. Epub 2011 Dec 19.
Abstract
Persistent infection with high-risk HPV is the etiologic agent associated with the development of cervical cancer (CC) development. However, environmental, social, epidemiological, genetic, and host factors may have a joint influence on the risk of disease progression. Cervical lesions caused by HPV infection can be removed naturally by the host immune response and only a small percentage may progress to cancer; thus, the immune response is essential for the control of precursor lesions and CC. We present a review of recent research on the molecular mechanisms that allow HPV-infected cells to evade immune surveillance and potential targets of molecular therapy to inhibit tumor immune escape.
摘要
高危型 HPV 的持续感染是与宫颈癌 (CC) 发展相关的病因。然而，环境、社会、流行病学、遗传和宿主因素可能对疾病进展的风险有共同影响。HPV 感染引起的宫颈病变可以被宿主免疫反应自然清除，只有一小部分可能进展为癌症；因此，免疫反应对于控制癌前病变和 CC 是至关重要的。我们综述了最近关于 HPV 感染细胞逃避免疫监视的分子机制以及抑制肿瘤免疫逃逸的分子治疗潜在靶点的研究。
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