The cell cycle and drug discovery: the promise and the hope

被引:34
作者
Brooks, G
La Thangue, NB
机构
[1] Profilix Ltd, Abingdon OX14 4RY, Oxon, England
[2] Univ Reading, Sch Anim & Microbial Sci, Reading RG6 6AJ, Berks, England
[3] Univ Glasgow, Div Biochem & Mol Biol, Glasgow G12 8QQ, Lanark, Scotland
关键词
D O I
10.1016/S1359-6446(99)01400-2
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In recent years, there have been major developments in the understanding of the cell cycle. It is now known that normal cellular proliferation is tightly regulated by the activation and deactivation of a series of proteins that constitute the cell cycle machinery. The expression and activity of components of the cell cycle can be altered during the development of a variety of diseases where aberrant proliferation contributes to the pathology of the illness. Apart from yielding a new source of untapped therapeutic targets, it is likely that manipulating the activity of such proteins in diseased states will provide an important route for treating proliferative disorders, and the opportunity to develop a novel class of future medicines.
引用
收藏
页码:455 / 464
页数:10
相关论文
共 96 条
[11]   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
[12]   Adenovirus-mediated p53 gene transfer in patients with advanced recurrent head and neck squamous cell carcinoma [J].
Clayman, GL ;
El-Naggar, AK ;
Lippman, SM ;
Henderson, YC ;
Frederick, M ;
Merritt, JA ;
Zumstein, LA ;
Timmons, TM ;
Liu, TJ ;
Ginsberg, L ;
Roth, JA ;
Hong, WK ;
Bruso, P ;
Goepfert, H .
JOURNAL OF CLINICAL ONCOLOGY, 1998, 16 (06) :2221-2232
[13]  
Coleman RL, 1997, SEMIN ONCOL, V24, pS55
[14]  
Collecchi P, 1999, INT J CANCER, V84, P139, DOI 10.1002/(SICI)1097-0215(19990420)84:2<139::AID-IJC8>3.0.CO
[15]  
2-Y
[16]  
Creemers GJ, 1997, SEMIN ONCOL, V24, pS42
[17]   TRANSCRIPTIONAL ACTIVATION BY P53 CORRELATES WITH SUPPRESSION OF GROWTH BUT NOT TRANSFORMATION [J].
CROOK, T ;
MARSTON, NJ ;
SARA, EA ;
VOUSDEN, KH .
CELL, 1994, 79 (05) :817-827
[18]   MICE DEFICIENT FOR P53 ARE DEVELOPMENTALLY NORMAL BUT SUSCEPTIBLE TO SPONTANEOUS TUMORS [J].
DONEHOWER, LA ;
HARVEY, M ;
SLAGLE, BL ;
MCARTHUR, MJ ;
MONTGOMERY, CA ;
BUTEL, JS ;
BRADLEY, A .
NATURE, 1992, 356 (6366) :215-221
[19]   The regulation of E2F by pRB-family proteins [J].
Dyson, N .
GENES & DEVELOPMENT, 1998, 12 (15) :2245-2262
[20]   Balloon angioplasty for the treatment of coronary in-stent restenosis: Immediate results and 6-month angiographic recurrent restenosis rate [J].
Eltchaninoff, H ;
Koning, R ;
Tron, C ;
Gupta, V ;
Cribier, A .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1998, 32 (04) :980-984