E Conseiller, L Debussche, D Landais, C Venot, M Maratrat, V Sierra, B Tocque, L Bracco
J Clin Invest.
1998;
101(1):120–127
doi:10.1172/JCI1140
This article Copyright © 1998, The American Society for Clinical Investigation
Abstract
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T
he clinical potential of the p53 tumor suppressor gene is being evaluated currently for gene therapy of cancer. We have built a variant of wild-type p53, chimeric tumor suppressor 1 (CTS1), in which we have replaced the domains that mediate its inactivation. CTS1 presents some very interesting properties: (a) enhanced transcriptional activity; (b) resistance to the inactivation by oncogenic forms of p53; (c) resistance to the inactivation by MDM2; (d) lower sensitivity to E6-induced degradation; (e) ability to suppress cell growth; and (f ) faster induction of apoptosis. Thus, CTS1 is an improved tumor suppressor and an alternative for the treatment of wild-type p53-resistant human tumors by gene therapy.
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