Oncogenic activities of human papillomaviruses

被引:276
作者
McLaughlin-Drubin, Margaret E. [1 ]
Muenger, Karl
机构
[1] Brigham & Womens Hosp, Div Infect Dis, Channing Labs, Boston, MA 02115 USA
关键词
HPV; Cervical cancer; p53; Retinoblastoma; Genomic instability; TYPE-16; E7; ONCOPROTEIN; TUMOR-NECROSIS-FACTOR; SEXUALLY-TRANSMITTED-DISEASES; PRIMARY HUMAN KERATINOCYTES; ADENOVIRUS E1A PROTEINS; HPV TYPE DISTRIBUTION; E6; RETINOBLASTOMA PROTEIN; CELL-CYCLE; CENTROSOME DUPLICATION;
D O I
10.1016/j.virusres.2009.06.008
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Infectious etiologies for certain human cancers have long been suggested by epidemiological studies and studies with experimental animals. Important support for this concept came from the discovery by Harald zur Hausen's group that human cervical carcinoma almost universally contains certain "highrisk" human papillomavirus (HPV) types. Over the years, much has been learned about the carcinogenic activities of high-risk HPVs. These studies have revealed that two viral proteins, E6 and E7, that are consistently expressed in HPV-associated carcinomas, are necessary for induction and maintenance of the transformed phenotype. Hence, HPV-associated tumors are unique amongst human solid tumors in that they are universally caused by exposure to the same, molecularly defined oncogenic agents, and the molecular signal transduction pathways subverted by these viral transforming agents are frequently disrupted in other, non-virus-associated human cancers. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:195 / 208
页数:14
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