Paths of FGFR-driven tumorigenesis

Cell Cycle. 2009 Feb 15;8(4):580-8. doi: 10.4161/cc.8.4.7657. Epub 2009 Feb 18.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cell Communication
  • Disease Progression
  • Epithelial Cells / physiology
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Neovascularization, Pathologic
  • Prostatic Neoplasms* / metabolism
  • Prostatic Neoplasms* / pathology
  • Prostatic Neoplasms* / physiopathology
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Protein-Tyrosine Kinases / metabolism
  • Receptors, Androgen / metabolism
  • Receptors, Fibroblast Growth Factor / genetics
  • Receptors, Fibroblast Growth Factor / metabolism*
  • Signal Transduction / physiology*
  • Stromal Cells / physiology


  • Protein Isoforms
  • Receptors, Androgen
  • Receptors, Fibroblast Growth Factor
  • Protein-Tyrosine Kinases