Manipulation of the tumor suppressor p53 for potentiating cancer therapy

被引:33
作者
Haupt, S
Haupt, Y [1 ]
机构
[1] Hebrew Univ Jerusalem, Sch Pharm, Dept Pharmaceut, IL-91120 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Hadassah Med Sch, Lautenberg Ctr Gen & Tumor Immunol, IL-91120 Jerusalem, Israel
基金
以色列科学基金会;
关键词
p53; Mdm2; therapy; DNA damage; small molecules;
D O I
10.1016/j.semcancer.2004.04.003
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The tumor suppressor p53 is a linchpin in the regulation of appropriate cellular responses to various stress conditions. Inactivation of the functions of this critical participant can have diabolical consequences, in particular the development of malignant diseases. Elicitation of appropriate p53 functions is an attractive strategy for combating cancer. Triggering p53 responses, reconstituting p53 activities through gene therapy, coercing mutant p53 to perform normal functions, manipulating p53 regulators, and activating p53 effectors are all approaches that are currently being developed. Here, we will overview 'p53-based' strategies for fighting cancer, both those under clinical trial and recent innovative concepts. (C) 2004 Elsevier Ltd. All rights reserved.
引用
收藏
页码:244 / 252
页数:9
相关论文
共 80 条
[1]  
Abarzua P, 1996, ONCOGENE, V13, P2477
[2]   Proteasome inhibition in cancer: Development of PS-341 [J].
Adams, J .
SEMINARS IN ONCOLOGY, 2001, 28 (06) :613-619
[3]   Aib-based peptide backbone as scaffolds for helical peptide mimics [J].
Banerjee, R ;
Basu, G ;
Chène, P ;
Roy, S .
JOURNAL OF PEPTIDE RESEARCH, 2002, 60 (02) :88-94
[4]   ASPP1 and ASPP2: Common activators of p53 family members [J].
Bergamaschi, D ;
Samuels, Y ;
Jin, BQ ;
Duraisingham, S ;
Crook, T ;
Lu, X .
MOLECULAR AND CELLULAR BIOLOGY, 2004, 24 (03) :1341-1350
[5]   p53 polymorphism influences response in cancer chemotherapy via modulation of p73-dependent apoptosis [J].
Bergamaschi, D ;
Gasco, M ;
Hiller, L ;
Sullivan, A ;
Syed, N ;
Trigiante, G ;
Yulug, I ;
Merlano, M ;
Numico, G ;
Comino, A ;
Attard, M ;
Reelfs, O ;
Gusterson, B ;
Bell, AK ;
Heath, V ;
Tavassoli, M ;
Farrell, PJ ;
Smith, P ;
Lu, X ;
Crook, T .
CANCER CELL, 2003, 3 (04) :387-402
[6]   Effect of mutated TP53 on response of advanced breast cancers to high-dose chemotherapy [J].
Bertheau, P ;
Plassa, F ;
Espié, M ;
Turpin, E ;
de Roquancourt, A ;
Marty, M ;
Lerebours, F ;
Beuzard, Y ;
Janin, A ;
de Thé, H .
LANCET, 2002, 360 (9336) :852-854
[7]   Mutant conformation of p53 translated in vitro or in vivo requires functional HSP90 [J].
Blagosklonny, MV ;
Toretsky, J ;
Bohen, S ;
Neckers, L .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (16) :8379-8383
[8]  
BLAGOSKLONNY MV, 1995, ONCOGENE, V11, P933
[9]   Mutant p53 gain of function: differential effects of different p53 mutants on resistance of cultured cells to chemotherapy [J].
Blandino, G ;
Levine, AJ ;
Oren, M .
ONCOGENE, 1999, 18 (02) :477-485
[10]   Wild-type p53 gene transfer is not detrimental to normal cells in vivo:: implications for tumor gene therapy [J].
Bossi, G ;
Mazzaro, G ;
Porrello, A ;
Crescenzi, M ;
Soddu, S ;
Sacchi, A .
ONCOGENE, 2004, 23 (02) :418-425