Human Papillomavirus Infections: Warts or Cancer?

被引：24

作者：

Chow, Louise T. ^{[1
]}

Broker, Thomas R. ^{[1
]}

机构：

[1] Univ Alabama Birmingham, Dept Biochem & Mol Genet, Birmingham, AL 35294 USA

来源：

COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY | 2013年 / 5卷 / 07期

关键词：

CERVICAL INTRAEPITHELIAL NEOPLASIA; PROMOTER METHYLATION ANALYSIS; CELLULAR FUSION TRANSCRIPTS; TYPE-16; E7; ONCOPROTEIN; DNA-DAMAGE RESPONSE; HIGH-RISK; S-PHASE; P21CIP1; PROTEIN; LIFE-CYCLE; POSTTRANSCRIPTIONAL INDUCTION;

D O I：

10.1101/cshperspect.a012997

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Human papillomaviruses (HPVs) are prevalent pathogens of mucosal and cutaneous epithelia. Productive infections of squamous epithelia lead to benign hyperproliferative warts, condylomata, or papillomas. Persistent infections of the anogenital mucosa by high-risk HPV genotypes 16 and 18 and closely related types can infrequently progress to high-grade intraepithelial neoplasias, carcinomas-in-situ, and invasive cancers in women and men. HPV-16 is also associated with a fraction of head and neck cancers. We discuss the interactions of the mucosotropic HPVs with the host regulatory proteins and pathways that lead to benign coexistence and enable HPV DNA amplification or, alternatively, to cancers that no longer support viral production.

引用

页数：17

共 142 条

[1] The X-ray structure of the papillomavirus helicase in complex with its molecular matchmaker E2 [J].

Abbate, EA ;

Berger, JM ;

Botchan, MR .

GENES & DEVELOPMENT, 2004, 18 (16) :1981-1996

[2] Conditionally activated E7 proteins of high-risk and low-risk human papillomaviruses induce S phase in postmitotic, differentiated human keratinocytes [J].

Banerjee, N. Sanjib ;

Genovese, Nicholas J. ;

Noya, Francisco ;

Chien, Wei-Ming ;

Broker, Thomas R. ;

Chow, Louise T. .

JOURNAL OF VIROLOGY, 2006, 80 (13) :6517-6524

[3] Human Papillomavirus (HPV) E7 Induces Prolonged G2 following S Phase Reentry in Differentiated Human Keratinocytes [J].

Banerjee, N. Sanjib ;

Wang, Hsu-Kun ;

Broker, Thomas R. ;

Chow, Louise T. .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2011, 286 (17) :15473-15482

[4] HPV16 E5 affects the KGFR/FGFR2b-mediated epithelial growth through alteration of the receptor expression, signaling and endocytic traffic [J].

Belleudi, F. ;

Leone, L. ;

Purpura, V. ;

Cannella, F. ;

Scrofani, C. ;

Torrisi, M. R. .

ONCOGENE, 2011, 30 (50) :4963-4976

[5]

Bernard HU, 2002, ANTIVIR THER, V7, P219

[6] Regulation of immune responses to HPVinfection and during HPV-directed immunotherapy [J].

Bhat, Purnima ;

Mattarollo, Stephen R. ;

Gosmann, Christina ;

Frazer, Ian H. ;

Leggatt, Graham R. .

IMMUNOLOGICAL REVIEWS, 2011, 239 :85-98

[7] Cyclophilins Facilitate Dissociation of the Human Papillomavirus Type 16 Capsid Protein L1 from the L2/DNA Complex following Virus Entry [J].

Bienkowska-Haba, Malgorzata ;

Williams, Carlyn ;

Kim, Seong Man ;

Garcea, Robert L. ;

Sapp, Martin .

JOURNAL OF VIROLOGY, 2012, 86 (18) :9875-9887

[8] Distinct human papillomavirus type 16 methylomes in cervical cells at different stages of premalignancy [J].

Brandsma, Janet L. ;

Sun, Ying ;

Lizardi, Paul M. ;

Tuck, David P. ;

Zelterman, Daniel ;

Haines, G. Kenneth, III ;

Martel, Maritza ;

Harigopal, Malini ;

Schofield, Kevin ;

Neapolitano, Matthew .

VIROLOGY, 2009, 389 (1-2) :100-107

[9] The clinical importance of understanding the evolution of papillomaviruses [J].

Bravo, Ignacio G. ;

de Sanjose, Silvia ;

Gottschling, Marc .

TRENDS IN MICROBIOLOGY, 2010, 18 (10) :432-438

[10]

BROKER TR, 1989, CANCER CEL, V7, P197

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