Angiogenesis-related pathways in the pathogenesis of ovarian cancer

Int J Mol Sci. 2013 Jul 30;14(8):15885-909. doi: 10.3390/ijms140815885.

Abstract

Ovarian Cancer represents the most fatal type of gynecological malignancies. A number of processes are involved in the pathogenesis of ovarian cancer, especially within the tumor microenvironment. Angiogenesis represents a hallmark phenomenon in cancer, and it is responsible for tumor spread and metastasis in ovarian cancer, among other tumor types, as it leads to new blood vessel formation. In recent years angiogenesis has been given considerable attention in order to identify targets for developing effective anti-tumor therapies. Growth factors have been identified to play key roles in driving angiogenesis and, thus, the formation of new blood vessels that assist in "feeding" cancer. Such molecules include the vascular endothelial growth factor (VEGF), the platelet derived growth factor (PDGF), the fibroblast growth factor (FGF), and the angiopoietin/Tie2 receptor complex. These proteins are key players in complex molecular pathways within the tumor cell and they have been in the spotlight of the development of anti-angiogenic molecules that may act as stand-alone therapeutics, or in concert with standard treatment regimes such as chemotherapy. The pathways involved in angiogenesis and molecules that have been developed in order to combat angiogenesis are described in this paper.

Publication types

  • Review

MeSH terms

  • Angiogenesis Inhibitors / therapeutic use
  • Female
  • Fibroblast Growth Factors / metabolism
  • Humans
  • Neovascularization, Pathologic*
  • Ovarian Neoplasms / drug therapy
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology*
  • Platelet-Derived Growth Factor / metabolism
  • Receptor, TIE-2 / metabolism
  • Signal Transduction
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Angiogenesis Inhibitors
  • Platelet-Derived Growth Factor
  • Vascular Endothelial Growth Factor A
  • Fibroblast Growth Factors
  • Receptor, TIE-2