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Ecancermedicalscience. 2015 Apr 29;9:526. doi: 10.3332/ecancer.2015.526. eCollection 2015.

Role of human papillomaviruses in carcinogenesis.

Author information

1
Department of Biological Sciences, Molecular and Computational Biology, University of Southern California, Los Angeles, CA 90089, USA.
2
Infections and Cancer Biology Group, International Agency for Research on Cancer, 150 cours Albert Thomas, 69008 Lyon, France.
3
IFOM-IEO Campus, Via Adamello 16, 20139 Milan, Italy.

Abstract

The human papillomavirus (HPV) family comprises more than 170 different types that preferentially infect the mucosa of the genitals, upper-respiratory tract, or the skin. The 'high-risk HPV type', a sub-group of mucosal HPVs, is the cause of approximately 5% of all human cancers, which corresponds to one-third of all virus-induced tumours. Within the high-risk group, HPV16 is the most oncogenic type, being responsible for approximatively 50% of all worldwide cervical cancers. Many studies suggest that, in addition to the high-risk mucosal HPV types, certain cutaneous HPVs also have a role in the development of non-melanoma skin cancer (NMSC). Functional studies on the HPV early gene products showed that E6 and E7 play a key role in carcinogenesis. These two proteins use multiple mechanisms to evade host immune surveillance, allowing viral persistence, and to deregulate cell cycle and apoptosis control, thus facilitating the accumulation of DNA damage and ultimately cellular transformation. The demonstration that high-risk HPV types are the etiological agents of cervical cancer allowed the implementation in the clinical routine of novel screening strategies for cervical lesions, as well as the development of a very efficient prophylactic vaccine. Because of these remarkable achievements, there is no doubt that in the coming decades we will witness a dramatic reduction of cervical cancer incidence worldwide.

KEYWORDS:

HPV vaccines; carcinogenesis; papillomavirus

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