Mutant KRAS, chromosomal instability and prognosis in colorectal cancer

被引:67
作者
Castagnola, P [1 ]
Giaretti, W [1 ]
机构
[1] Natl Inst Canc Res, I-16132 Genoa, Italy
来源
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2005年 / 1756卷 / 02期
关键词
KRAS; prognosis; colorectal cancer; chromosomal instability;
D O I
10.1016/j.bbcan.2005.06.003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The RAS gene family provides a global effect on gene expression by encoding small GTP-binding proteins which act as molecular switches connecting extracellular signals with nuclear transcription factors. While wild type RAS proteins are switched off shortly after activation, mutant RAS proteins remain constitutively activated leading to complex interactions among their downstream effectors. For some human tumor types, these interactions were shown to contribute to cancer genesis and progression by inducing changes in cell survival, apoptosis, angiogenesis, invasion and metastasis. This review addresses the controversial link of KRAS mutations in colorectal cancer with chromosomal instability and patient prognosis. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:115 / 125
页数:11
相关论文
共 208 条
[61]   Human papillomaviruses and centrosome duplication errors:: modeling the origins of genomic instability [J].
Duensing, S ;
Münger, K .
ONCOGENE, 2002, 21 (40) :6241-6248
[62]  
Duesberg P, 2004, CELL CYCLE, V3, P823
[63]   Aneuploidy, the primary cause of the multilateral genomic instability of neoplastic and preneoplastic cells [J].
Duesberg, P ;
Fabarius, A ;
Hehlmann, R .
IUBMB LIFE, 2004, 56 (02) :65-81
[64]   Stabilization of cyclin D1 mRNA via the phosphatidylinositol 3-kinase pathway in MCF-7 human breast cancer cells [J].
Dufourny, B ;
van Teeffelen, HAAM ;
Hamelers, IHL ;
Sussenbach, JS ;
Steenbergh, PH .
JOURNAL OF ENDOCRINOLOGY, 2000, 166 (02) :329-338
[65]   C-KI-RAS activation and the biological behaviour of proximal and distal colonic adenocarcinomas [J].
Elnatan, J ;
Goh, HS ;
Smith, DR .
EUROPEAN JOURNAL OF CANCER, 1996, 32A (03) :491-497
[66]   Chromosome number and structure both are markedly stable in RER colorectal cancers and are not destabilized by mutation of p53 [J].
Eshleman, JR ;
Casey, G ;
Kochera, ME ;
Sedwick, WD ;
Swinler, SE ;
Veigl, ML ;
Willson, JKV ;
Schwartz, S ;
Markowitz, SD .
ONCOGENE, 1998, 17 (06) :719-725
[67]   K-ras and p16 aberrations confer poor prognosis in human colorectal cancer [J].
Esteller, M ;
González, S ;
Risques, RA ;
Marcuello, E ;
Mangues, R ;
Germà, JR ;
Herman, JG ;
Capellà, G ;
Peinado, MA .
JOURNAL OF CLINICAL ONCOLOGY, 2001, 19 (02) :299-304
[68]   A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS [J].
FEARON, ER ;
VOGELSTEIN, B .
CELL, 1990, 61 (05) :759-767
[69]   c-MYC overexpression in Ba/F3 cells simultaneously elicits genomic instability and apoptosis [J].
Fest, T ;
Mougey, V ;
Dalstein, V ;
Hagerty, M ;
Milette, D ;
Silva, S ;
Mai, S .
ONCOGENE, 2002, 21 (19) :2981-2990
[70]   Mutations in the APC tumour suppressor gene cause chromosomal instability [J].
Fodde, R ;
Kuipers, J ;
Rosenberg, C ;
Smits, R ;
Kielman, M ;
Gaspar, C ;
van Es, JH ;
Bruekel, C ;
Wiegant, J ;
Giles, RH ;
Clevers, H .
NATURE CELL BIOLOGY, 2001, 3 (04) :433-438