Interview with the retinoblastoma family members: Do they help each other?

被引:15
作者
Tonini, T
Hillson, C
Claudio, PP
机构
[1] Temple Univ, Ctr Biotechnol, Coll Sci & Technol, Sbarro Inst Canc Res & Mol Med, Philadelphia, PA 19122 USA
[2] Univ Siena, Ist Anat & Istol Patol, I-53100 Siena, Italy
[3] Univ Naples Federico II, Dept Sci Odontostomol & Maxillo Facciali, Naples, Italy
关键词
D O I
10.1002/jcp.10117
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The ultimate destiny of a cell to undergo division, differentiation, survival, and death results from an intricate balance between multiple regulators including oncogenes, tumor suppressor genes, and cell cycle associated proteins. Deregulation of the cell cycle machinery switches the phenotype from a normal cell to a cancerous cell. Fundamental alterations of tumor suppressor genes may result in an unregulated cell cycle with the accumulation of mutations and eventual neoplastic transformation. As such, one may define cancer as a genetic disease of the cell cycle. in this review, we will emphasize our current understanding of how the cell cycle machinery maintains cellular homeostasis by studying the consequences of its deregulation. (C) 2002 Wiley-Liss, Inc.
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页码:138 / 150
页数:13
相关论文
共 152 条
[1]  
AJCHENBAUM F, 1993, J BIOL CHEM, V268, P4113
[2]  
Baldi A, 1997, CLIN CANCER RES, V3, P1691
[3]  
BALDREE LA, 1993, AM J KIDNEY DIS, V22, P1
[4]   CYCLIN-A AND THE RETINOBLASTOMA GENE-PRODUCT COMPLEX WITH A COMMON TRANSCRIPTION FACTOR [J].
BANDARA, LR ;
ADAMCZEWSKI, JP ;
HUNT, T ;
LATHANGUE, NB .
NATURE, 1991, 352 (6332) :249-251
[5]   Cell cycle regulation by the retinoblastoma family of growth inhibitory proteins [J].
Beijersbergen, RL ;
Bernards, R .
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER, 1996, 1287 (2-3) :103-120
[6]   REGULATION OF THE RETINOBLASTOMA PROTEIN-RELATED P107 BY G(1) CYCLIN COMPLEXES [J].
BEIJERSBERGEN, RL ;
CARLEE, L ;
KERKHOVEN, RM ;
BERNARDS, R .
GENES & DEVELOPMENT, 1995, 9 (11) :1340-1353
[7]  
Berry DE, 1996, ONCOGENE, V12, P1809
[8]  
Bonetto F, 1999, J CELL BIOCHEM, V75, P698, DOI 10.1002/(SICI)1097-4644(19991215)75:4<698::AID-JCB15>3.0.CO
[9]  
2-7
[10]   How tumors become angiogenic [J].
Bouck, N ;
Stellmach, V ;
Hsu, SC .
ADVANCES IN CANCER RESEARCH, VOL 69, 1996, 69 :135-174