Fibroblast growth factor signalling: from development to cancer

被引:2109
作者
Turner, Nicholas [1 ,2 ]
Grose, Richard [3 ]
机构
[1] Inst Canc Res, Breakthrough Breast Canc Res Ctr, London SW3 6JB, England
[2] Royal Marsden Hosp, London SW3 6JJ, England
[3] Queen Mary Univ London, Barts & London Sch Med & Dent, Inst Canc, London EC1M 6BQ, England
基金
英国惠康基金; 英国医学研究理事会;
关键词
GENOME-WIDE ASSOCIATION; FACTOR RECEPTOR-3 FGFR3; PROTEIN-KINASE-C; T-CELL LYMPHOMA; MULTIPLE-MYELOMA; ACTIVATING MUTATIONS; BREAST-CANCER; THERAPEUTIC TARGET; BLADDER-CARCINOMA; TUMOR-GROWTH;
D O I
10.1038/nrc2780
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Fibroblast growth factors (FGFs) and their receptors control a wide range of biological functions, regulating cellular proliferation, survival, migration and differentiation. Although targeting FGF signalling as a cancer therapeutic target has lagged behind that of other receptor tyrosine kinases, there is now substantial evidence for the importance of FGF signalling in the pathogenesis of diverse tumour types, and clinical reagents that specifically target the FGFs or FGF receptors are being developed. Although FGF signalling can drive tumorigenesis, in different contexts FGF signalling can mediate tumour protective functions; the identification of the mechanisms that underlie these differential effects will be important to understand how FGF signalling can be most appropriately therapeutically targeted.
引用
收藏
页码:116 / 129
页数:14
相关论文
共 189 条
[31]  
Courjal F, 1997, CANCER RES, V57, P4360
[32]   Tyrosine kinase fusion genes in chronic myeloproliferative diseases [J].
Cross, NCP ;
Reiter, A .
LEUKEMIA, 2002, 16 (07) :1207-1212
[33]   A secreted FGF-binding protein can serve as the angiogenic switch in human cancer [J].
Czubayko, F ;
LiaudetCoopman, EDE ;
Aigner, A ;
Tuveson, AT ;
Berchem, GJ ;
Wellstein, A .
NATURE MEDICINE, 1997, 3 (10) :1137-1140
[34]   Mechanisms underlying differential responses to FGF signaling [J].
Dailey, L ;
Ambrosetti, D ;
Mansukhani, A ;
Basilico, C .
CYTOKINE & GROWTH FACTOR REVIEWS, 2005, 16 (02) :233-247
[35]   MMTV-Fgf8 transgenic mice develop mammary and salivary gland neoplasia and ovarian stromal hyperplasia [J].
Daphna-Iken, D ;
Shankar, DB ;
Lawshé, A ;
Ornitz, DM ;
Shackleford, GM ;
MacArthur, CA .
ONCOGENE, 1998, 17 (21) :2711-2717
[36]   Loss of Sef (similar expression to FGF) expression is associated with high grade and metastatic prostate cancer [J].
Darby, S. ;
Sahadevan, K. ;
Khan, M. M. ;
Robson, C. N. ;
Leung, H. Y. ;
Gnanapragasam, V. J. .
ONCOGENE, 2006, 25 (29) :4122-4127
[37]   INVOLVEMENT OF PROTEIN KINASE-C IN THE MITOGENIC AND CHEMOTAXIS EFFECTS OF BASIC FIBROBLAST GROWTH-FACTOR ON BOVINE CEREBRAL-CORTEX CAPILLARY ENDOTHELIAL-CELLS [J].
DAVIET, I ;
HERBERT, JM ;
MAFFRAND, JP .
FEBS LETTERS, 1990, 259 (02) :315-317
[38]  
De Moerlooze L, 2000, DEVELOPMENT, V127, P483
[39]   Targeting FGF19 inhibits tumor growth in colon cancer xenograft and FGF19 transgenic hepatocellular carcinoma models [J].
Desnoyers, Lr ;
Pai, R. ;
Ferrando, Re ;
Hotzel, K. ;
Le, T. ;
Ross, J. ;
Carano, R. ;
D'Souza, A. ;
Qing, J. ;
Mohtashemi, I. ;
Ashkenazi, A. ;
French, Dm .
ONCOGENE, 2008, 27 (01) :85-97
[40]   Mutant fibroblast growth factor receptor 3 induces intracellular signaling and cellular transformation in a cell type- and mutation-specific manner [J].
di Martino, E. ;
L'Hote, C. G. ;
Kennedy, W. ;
Tomlinson, D. C. ;
Knowles, M. A. .
ONCOGENE, 2009, 28 (48) :4306-4316