p53 as a target for anti-cancer drug development

被引：80

作者：

Bouchet, Benjamin Pierre ^{[1
]}

de Fromentel, Claude Caron ^{[1
]}

Puisieux, Alain ^{[1
]}

Galmarini, Carlos Maria ^{[1
]}

机构：

[1] Ctr Leon Berard, INSERM, U590, F-69373 Lyon 08, France

来源：

CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY | 2006年 / 58卷 / 03期

关键词：

p53; protein; apoptosis; mutation; prognosis; gene therapy; ONYX-015;

D O I：

10.1016/j.critrevonc.2005.10.005

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Loss of p53 function compromises genetic homeostasis in cells exhibiting deregulated DNA replication and/or DNA damage, and prevents normal cytotoxic responses to cancer therapies. Genetic and pharmacological approaches are being developed with the ultimate goal of restoring or controlling p53 functions in cancer patients. Progress has recently been made in the clinical use of replication-deficient virus carrying wt-TP53 (Ad5CMV-p53) and/or cancer-selective oncolytic adenoviruses (ONYX-015). These strategies demonstrated clinical activity as monotherapy and were synergistic with traditional chemotherapy agents in the treatment of some types of cancer. In addition, pharmacological methods are under development to either stimulate wild-type p53 protein function, or induce p53 mutant proteins to resume wild-type functions. These methods are based on small chemicals (CP-31388, PRIMA-1), peptides (CDB3) or single-chain Fv antibody fragments corresponding to defined p53 domains. Here, we discuss the mechanisms underlying these approaches and their perspectives for cancer therapy. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

引用

页码：190 / 207

页数：18

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