The challenge of p53: Linking biochemistry, biology, and patient management

被引:14
作者
Bray, SE [1 ]
Schorl, C [1 ]
Hall, PA [1 ]
机构
[1] Univ Dundee, Ninewells Hosp & Med Sch, Dept Cellular & Mol Pathol, Dundee DD1 9SY, Scotland
关键词
p53; stress responses; physiology; biochemistry; therapy;
D O I
10.1002/stem.160248
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Abnormalities of the p53 tumor suppressor gene are the single most common molecular abnormality seen in human cancer, Considerable evidence indicates that the product of this gene has critical roles in coordinating the response of cells to a diverse range of environmental stresses, At present, there is a gamut of biochemical properties and interactions ascribed to p53, but the in vivo physiological relevance of many of these remains uncertain. The development of clinical applications and novel therapeutic strategies utilizing our knowledge of p53 is contingent upon bridging the gap between rigorous biochemistry and holistic in vivo studies.
引用
收藏
页码:248 / 260
页数:13
相关论文
共 121 条
[21]   GROWTH-FACTOR MODULATION OF P53-MEDIATED GROWTH ARREST VERSUS APOPTOSIS [J].
CANMAN, CE ;
GILMER, TM ;
COUTTS, SB ;
KASTAN, MB .
GENES & DEVELOPMENT, 1995, 9 (05) :600-611
[22]   MAPPING OF THE P53 AND MDM-2 INTERACTION DOMAINS [J].
CHEN, JD ;
MARECHAL, V ;
LEVINE, AJ .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (07) :4107-4114
[23]   p53 levels, functional domains, and DNA damage determine the extent of the apoptotic response of tumor cells [J].
Chen, XB ;
Ko, LJ ;
Jayaraman, L ;
Prives, C .
GENES & DEVELOPMENT, 1996, 10 (19) :2438-2451
[24]  
CHO Y, 1994, SCIENCE, V265, P1353
[25]  
CLARKE AR, 1994, ONCOGENE, V9, P1767
[26]   THYMOCYTE APOPTOSIS INDUCED BY P53-DEPENDENT AND INDEPENDENT PATHWAYS [J].
CLARKE, AR ;
PURDIE, CA ;
HARRISON, DJ ;
MORRIS, RG ;
BIRD, CC ;
HOOPER, ML ;
WYLLIE, AH .
NATURE, 1993, 362 (6423) :849-852
[27]   Tumour-suppressor genes - Killer in search of a motive? [J].
Clurman, B ;
Groudine, M .
NATURE, 1997, 389 (6647) :122-123
[28]   DEMONSTRATION OF DNA-DAMAGE REPAIR IN INDIVIDUAL CELLS USING IN-SITU END LABELING - ASSOCIATION OF P53 WITH SITES OF DNA-DAMAGE [J].
COATES, PJ ;
SAVE, V ;
ANSARI, B ;
HALL, PA .
JOURNAL OF PATHOLOGY, 1995, 176 (01) :19-26
[29]   ATTENUATION OF P53 EXPRESSION PROTECTS AGAINST FOCAL ISCHEMIC DAMAGE IN TRANSGENIC MICE [J].
CRUMRINE, RC ;
THOMAS, AL ;
MORGAN, PF .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1994, 14 (06) :887-891
[30]   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