The human papillomavirus family and its role in carcinogenesis

被引:305
作者
Tommasino, Massimo [1 ]
机构
[1] Int Agcy Res Canc, World Hlth Org, Infect & Canc Biol Grp, F-69372 Lyon 08, France
关键词
Human papillomavirus; Cancer; E6 and E7 oncoproteins; Viral persistence; Cellular transformation; SQUAMOUS-CELL CARCINOMA; CUTANEOUS HUMAN PAPILLOMAVIRUSES; GAMMA HUMAN PAPILLOMAVIRUSES; NF-KAPPA-B; CERVICAL-CANCER; E7; ONCOPROTEIN; E6; SKIN-CANCER; TYPE-16; BETAPAPILLOMAVIRUS INFECTION;
D O I
10.1016/j.semcancer.2013.11.002
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Human papillomaviruses (HPVs) are a family of small double-stranded DNA viruses that have a tropism for the epithelia of the genital and upper respiratory tracts and for the skin. Approximately 150 HPV types have been discovered so far, which are classified into several genera based on their DNA sequence. Approximately 15 high-risk mucosal HPV types are clearly associated with cervical cancer; HPV16 and HPV18 are the most carcinogenic since they are responsible for approximately 50% and 20% of all cervical cancers worldwide, respectively. It is now also clear that these viruses are linked to a subset of other genital cancers, as well as head and neck cancers. Due to their high level of carcinogenic activity, HPV16 and HPV18 are the most studied HPV types so far. Biological studies have highlighted the key roles in cellular transformation of the products of two viral early genes, E6 and E7. Many of the mechanisms of E6 and E7 in subverting the regulation of fundamental cellular events have been fully characterized, contributing not only to our knowledge of how the oncogenic viruses promote cancer development but also to our understanding of basic cell biology. Despite HPV research resulting in extraordinary achievements in the last four decades, significantly improving the screening and prophylaxis of HPV-induced lesions, additional research is necessary to characterize the biology and epidemiology of the vast number of HPV types that have been poorly investigated so far, with a final aim of clarifying their potential roles in other human diseases. (C) 2013 Elsevier Ltd. All rights reserved.
引用
收藏
页码:13 / 21
页数:9
相关论文
共 123 条
[1]
Skin human papillomavirus type 38 alters p53 functions by accumulation of ΔNp73 [J].
Accardi, R ;
Dong, W ;
Smet, A ;
Cui, R ;
Hautefeuille, A ;
Gabet, AS ;
Sylla, BS ;
Gissmann, L ;
Hainaut, P ;
Tommasino, M .
EMBO REPORTS, 2006, 7 (03) :334-340
[2]
Epstein - Barr Virus Transforming Protein LMP-1 Alters B Cells Gene Expression by Promoting Accumulation of the Oncoprotein ΔNp73α [J].
Accardi, Rosita ;
Fathallah, Ikbal ;
Gruffat, Henri ;
Mariggio, Giuseppe ;
Le Calvez-Kelm, Florence ;
Voegele, Catherine ;
Bartosch, Birke ;
Hernandez-Vargas, Hector ;
McKay, James ;
Sylla, Bakary S. ;
Manet, Evelyne ;
Tommasino, Massimo .
PLOS PATHOGENS, 2013, 9 (03)
[3]
IκB Kinase β Promotes Cell Survival by Antagonizing p53 Functions through ΔNp73α Phosphorylation and Stabilization [J].
Accardi, Rosita ;
Scalise, Mariafrancesca ;
Gheit, Tarik ;
Hussain, Ishraq ;
Yue, Jiping ;
Carreira, Christine ;
Collino, Agnese ;
Indiveri, Cesare ;
Gissmann, Lutz ;
Sylla, Bakary S. ;
Tommasino, Massimo .
MOLECULAR AND CELLULAR BIOLOGY, 2011, 31 (11) :2210-2226
[4]
Sunlight and skin cancer: Inhibition of p53 mutations in UV-irradiated mouse skin by sunscreens [J].
Ananthaswamy, HN ;
Loughlin, SM ;
Cox, P ;
Evans, RL ;
Ullrich, SE ;
Kripke, ML .
NATURE MEDICINE, 1997, 3 (05) :510-514
[5]
[Anonymous], 2003, J NATL CANC I, DOI DOI 10.1093/0XF0RDJ0UR-NALS.JNCIM0N0GRAPHS.A003483
[6]
[Anonymous], INT J CANC
[7]
The epidemiology of UV induced skin cancer [J].
Armstrong, BK ;
Kricker, A .
JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY, 2001, 63 (1-3) :8-18
[8]
Human papillomaviruses are commonly found in normal skin of immunocompetent hosts [J].
Astori, G ;
Lavergne, D ;
Benton, C ;
Höckmayr, B ;
Egawa, K ;
Garbe, C ;
de Villiers, EM .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1998, 110 (05) :752-755
[9]
A novel repressive E2F6 complex containing the polycomb group protein, EPC1, that interacts with EZH2 in a proliferation-specific manner [J].
Attwooll, C ;
Oddi, S ;
Cartwright, P ;
Prosperini, E ;
Agger, K ;
Steensgaard, P ;
Wagener, C ;
Sardet, C ;
Moroni, MC ;
Helin, K .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (02) :1199-1208
[10]
Human tumour viruses and the deregulation of cell polarity in cancer [J].
Banks, Lawrence ;
Pim, David ;
Thomas, Miranda .
NATURE REVIEWS CANCER, 2012, 12 (12) :876-885