Current Oncology Reports

, Volume 12, Issue 2, pp 102–108

Vascular Endothelial Growth Factor Polymorphisms: Role in Response and Toxicity of Tyrosine Kinase Inhibitors

Authors

  • Susan A. J. Vaziri
    • Taussig Cancer Institute - R40Cleveland Clinic Foundation
  • Jenny Kim
    • Taussig Cancer Institute - R40Cleveland Clinic Foundation
  • Mahrukh K. Ganapathi
    • Taussig Cancer Institute - R40Cleveland Clinic Foundation
    • Taussig Cancer Institute - R40Cleveland Clinic Foundation
Article

DOI: 10.1007/s11912-010-0085-4

Cite this article as:
Vaziri, S.A.J., Kim, J., Ganapathi, M.K. et al. Curr Oncol Rep (2010) 12: 102. doi:10.1007/s11912-010-0085-4

Abstract

Angiogenesis is central to the growth of normal tissues and tumors. Inhibiting this pathway has been a strategy for drug development for tumors not responsive to most agents used in chemotherapy. Notably, signaling mediated by vascular endothelial growth factor (VEGF) is a key target because aberrant signaling via this pathway is frequently associated with neoangiogenesis in tumors. The drug-discovery effort to blunt VEGF signaling has led to the approval of bevacizumab and several receptor tyrosine kinase inhibitors (TKIs) that have shown efficacy in the clinical management of breast, colorectal, lung, and kidney cancer. Understanding the genetic variability in VEGF and VEGF receptor has led to identifying genotypic variations (single nucleotide polymorphisms [SNPs]) associated with treatment outcome and toxicity. Notably, identification of SNPs in VEGF associated with angiogenesis inhibitor treatment-induced hypertension and outcome provides exciting opportunities for personalized medicine to improve outcome and reduced toxicity with these novel TKIs.

Keywords

AngiogenesisTyrosine kinase inhibitorsHypertensionVEGF polymorphismOutcomeToxicity

Copyright information

© Springer Science+Business Media, LLC 2010