30 years and a long way into p53 research

被引:65
作者
Hainaut, Pierre [1 ]
Wiman, Klas G. [2 ]
机构
[1] Int Agcy Res Canc, F-69372 Lyon, France
[2] Karolinska Inst, Stockholm, Sweden
关键词
WILD-TYPE P53; CELLULAR TUMOR-ANTIGEN; MUTANT P53; P53-DEPENDENT APOPTOSIS; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; GENE-MUTATIONS; BINDING-SITE; DNA-BINDING; PROTEIN;
D O I
10.1016/S1470-2045(09)70198-6
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Among the 278 092 publications indexed into PubMed in 1979, a handful of articles stand out as the foundation of one of the most profound forays into the molecular basis of carcinogenesis: the discovery of the p53 tumour-suppressor protein. In the 30 years since then, understanding of p53 has progressed from obscure oncogene to key tumour-suppressor gene with clinical potential. Yet, p53 research has not followed a straight course. In this Historical Review, we describe how the 1979 discovery has shaped our view of the molecular basis of cancer, and identify some crucial steps ahead to transfer the wealth of knowledge accumulated on p53 into applications to cancer prevention and treatment.
引用
收藏
页码:913 / 919
页数:7
相关论文
共 101 条
[1]  
Ambs S, 1998, CANCER RES, V58, P334
[2]   CHROMOSOME-17 DELETIONS AND P53 GENE-MUTATIONS IN COLORECTAL CARCINOMAS [J].
BAKER, SJ ;
FEARON, ER ;
NIGRO, JM ;
HAMILTON, SR ;
PREISINGER, AC ;
JESSUP, JM ;
VANTUINEN, P ;
LEDBETTER, DH ;
BARKER, DF ;
NAKAMURA, Y ;
WHITE, R ;
VOGELSTEIN, B .
SCIENCE, 1989, 244 (4901) :217-221
[3]   MDM2 EXPRESSION IS INDUCED BY WILD TYPE-P53 ACTIVITY [J].
BARAK, Y ;
JUVEN, T ;
HAFFNER, R ;
OREN, M .
EMBO JOURNAL, 1993, 12 (02) :461-468
[4]   DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis [J].
Bartkova, J ;
Horejsi, Z ;
Koed, K ;
Krämer, A ;
Tort, F ;
Zieger, K ;
Guldberg, P ;
Sehested, M ;
Nesland, JM ;
Lukas, C ;
Orntoft, T ;
Lukas, J ;
Bartek, J .
NATURE, 2005, 434 (7035) :864-870
[5]   p53-mediated activation of miRNA34 candidate tumor-suppressor genes [J].
Bommer, Guido T. ;
Gerin, Isabelle ;
Feng, Ying ;
Kaczorowski, Andrew J. ;
Kuick, Rork ;
Love, Robert E. ;
Zhai, Yali ;
Giordano, Thomas J. ;
Qin, Zhaohui S. ;
Moore, Bethany B. ;
MacDougald, Ormond A. ;
Cho, Kathleen R. ;
Fearon, Eric R. .
CURRENT BIOLOGY, 2007, 17 (15) :1298-1307
[6]   p53 isoforms can regulate p53 transcriptional activity [J].
Bourdon, JC ;
Fernandes, K ;
Murray-Zmijewski, F ;
Liu, G ;
Diot, A ;
Xirodimas, DP ;
Saville, MK ;
Lane, DP .
GENES & DEVELOPMENT, 2005, 19 (18) :2122-2137
[7]   Restoration of the tumor suppressor function to mutant p53 by a low-molecular-weight compound [J].
Bykov, VJN ;
Issaeva, N ;
Shilov, A ;
Hultcrantz, M ;
Pugacheva, E ;
Chumakov, P ;
Bergman, J ;
Wiman, KG ;
Selivanova, G .
NATURE MEDICINE, 2002, 8 (03) :282-288
[8]   Activation of the ATM kinase by ionizing radiation and phosphorylation of p53 [J].
Canman, CE ;
Lim, DS ;
Cimprich, KA ;
Taya, Y ;
Tamai, K ;
Sakaguchi, K ;
Appella, E ;
Kastan, MB ;
Siliciano, JD .
SCIENCE, 1998, 281 (5383) :1677-1679
[9]   IDENTIFICATION AND PARTIAL CHARACTERIZATION OF NEW ANTIGENS FROM SIMIAN-VIRUS 40-TRANSFORMED MOUSE CELLS [J].
CHANG, C ;
SIMMONS, DT ;
MARTIN, MA ;
MORA, PT .
JOURNAL OF VIROLOGY, 1979, 31 (02) :463-471
[10]   CRYSTAL-STRUCTURE OF A P53 TUMOR-SUPPRESSOR DNA COMPLEX - UNDERSTANDING TUMORIGENIC MUTATIONS [J].
CHO, YJ ;
GORINA, S ;
JEFFREY, PD ;
PAVLETICH, NP .
SCIENCE, 1994, 265 (5170) :346-355