Paths of FGFR-driven tumorigenesis
Volume 8, Issue 4
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February 15, 2009
Pages 580 - 588http://dx.doi.org/10.4161/cc.8.4.7657
Authors: Victor D. Acevedo, Michael Ittmann and David M. Spencer View affiliations
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.
Received: December 11, 2008; Accepted: December 18, 2008