

Author: Pipas J.M. Levine A.J.
Publisher: Academic Press
ISSN: 1044-579X
Source: Seminars in Cancer Biology, Vol.11, Iss.1, 2001-02, pp. : 23-30
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
SV40 induces neoplastic transformation by disabling several key cellular growth regulatory circuits. Among these are the Rb- and p53-families of tumor suppressors. The multifunctional, virus-encoded large T antigen blocks the function of both Rb and p53. Large T antigen uses multiple mechanisms to block p53 activity, and this action contributes to tumorigenesis, in part, by blocking p53-mediated growth suppression and apoptosis. Since the p53 pathway is inactivated in most human tumors, T antigen/p53 interactions offer a possible mechanism by which SV40 contributes to human cancer.
Related content


Wild-Type p53 Overexpression: What Role in Tumorigenesis?
Gynecologic Oncology, Vol. 60, Iss. 3, 1996-03 ,pp. :




By Jinfeng Ma Kimura Wataru Sakurai Fumiaki Moriya Toshiyuki Takeshita Akiko Hirai Ichiro
International Journal of Gastrointestinal Cancer, Vol. 32, Iss. 2-3, 2002-12 ,pp. :

