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The disruption of cell cycle checkpoints by papillomavirus oncoproteins contributes to anogenital neoplasia
Author(s): Galloway DA, McDougall JK
Source: SEMINARS IN CANCER BIOLOGY    Volume: 7    Issue: 6    Pages: 309-315    Published: DEC 1996  
Times Cited: 53     References: 49     
Abstract: Human cancers are characterized by the failure of cell cycle checkpoints resulting in genetic instability. Human papillomaviruses contribute to the development of anogenital malignancies because the E6 and E7 oncoproteins from high risk HPV types are able to disrupt the integrity of these checkpoints. HPV 16 E7 prevents suprabasal cells from exiting the cell cycle, thus increasing the pool of replicating cells that are available for additional 'hits'. Cells that suffer DNA or chromosome damage are not eliminated because EG and E7 are able to bypass G1 and G2 damage-induced checkpoints. The activation, or inactivation, of additional cellular genes required for invasion and metastasis may not be a direct consequence of the E6/E7 oncoproteins. (C) 1997 Academic Press Ltd.
Document Type: Article
Language: English
Reprint Address: Galloway, DA (reprint author), FRED HUTCHINSON CANC RES CTR, PROGRAM CANC BIOL, 1100 FAIRVIEW AVE N, ROOM C1-105, POB 19024, SEATTLE, WA 98109 USA
Publisher: ACADEMIC PRESS LTD, 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX
Subject Category: Oncology
IDS Number: XR609
ISSN: 1044-579X
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