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Journal of Oncology
Volume 2012, Article ID 278312, 11 pages
Review Article

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

1Division of Chronic Infections and Cancer, Research Center for Infectious Diseases, Instituto Nacional de Salud Pública, Avenida Universidad No. 655, Cuernavaca 62100, Morelos, Mexico
2Universidad Politécnica del Estado de Morelos, Boulevard Cuauhnáhuac 566, Jiutepec 62550, Morelos, Mexico

Received 30 July 2011; Revised 27 September 2011; Accepted 28 September 2011

Academic Editor: Adhemar Longatto-Filho

Copyright © 2012 E. Guzmán-Olea et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.