Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development. (19th December 2011)

• Record Type: Journal Article
• Authors: Guzmán-Olea, E.; Bermúdez-Morales, V. H.; Peralta-Zaragoza, O.; Torres-Poveda, K.; Madrid-Marina, V.
• Other Names: Longatto-Filho Adhemar Academic Editor.
• Is Part Of: Journal of oncology. Volume 2012(2012)
• Publication Date: 2011-12-19
• Subjects: Oncology -- Research -- Periodicals; Tumors -- Periodicals; Neoplasms; Oncology -- Research; Tumors; Periodicals; Periodicals; 616.994
• DOI: 10.1155/2012/278312
• Languages: English
• ISSNs: 1687-8450

Abstract

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.