Paths of FGFR-driven tumorigenesis

被引：131
作者：
Acevedo, Victor D. [1 ,2 ]
Ittmann, Michael [3 ]
Spencer, David M. [1 ,2 ]
机构：
[1] Baylor Coll Med, Cell & Mol Biol Program, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA
[3] Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA
来源：
CELL CYCLE | 2009年 / 8卷 / 04期
关键词：
prostate cancer; fibroblast growth factor receptor (FGFR); chemical inducer of dimerization (CID); epithelial-mesenchymal transition (EMT); angiogenesis; androgen independence; FIBROBLAST-GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; RECEPTOR TYROSINE KINASE; PROSTATE-CANCER; ANDROGEN-RECEPTOR; TUMOR-GROWTH; ENDOTHELIAL-CELLS; INTRAEPITHELIAL NEOPLASIA; TRANSCRIPTION FACTOR; STRUCTURAL BASIS;
D O I：
10.4161/cc.8.4.7657
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Fibroblast growth factor receptors (FGFRs) comprise a subfamily of receptor tyrosine kinases (RTKs) that are master regulators of a broad spectrum of cellular and developmental processes, including apoptosis, proliferation, migration and angiogenesis. Due to their broad impact, FGFRs and other RTKs are highly regulated and normally only basally active. Deregulation of FGFR signaling by activating mutations or ligand/receptor overexpression could allow these receptors to become constitutively active, leading to cancer development, including both hematopoietic and solid tumors, such as breast, bladder and prostate carcinomas. In this review, we focus on potential modes of FGFR-mediated tumorigenesis, in particular, the role of FGFR1 during prostate cancer progression.
引用
收藏
页码：580 / 588
页数：9
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