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Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development

By E. Guzmán-Olea, V. H. Bermúdez-Morales, O. Peralta-Zaragoza, K. Torres-Poveda and V. Madrid-Marina

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

Topics: Review Article
Publisher: Hindawi Publishing Corporation
OAI identifier: oai:pubmedcentral.nih.gov:3246776
Provided by: PubMed Central

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