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Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development
Author(s) -
Eduardo Guzmán-Olea,
Víctor H. Bermúdez-Morales,
Oscar PeraltaZaragoza,
Kirvis Torres-Poveda,
Vicente MadridMarina
Publication year - 2011
Publication title -
journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 54
eISSN - 1687-8469
pISSN - 1687-8450
DOI - 10.1155/2012/278312
Subject(s) - immune system , medicine , mechanism (biology) , disease , cervical cancer , lesion , immunology , cancer , epidemiology , human papillomavirus , immune status , hpv infection , pathology , philosophy , epistemology
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.

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