Current Oncology Reports

, Volume 12, Issue 2, pp 102-108

First online:

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

  • Susan A. J. VaziriAffiliated withTaussig Cancer Institute - R40, Cleveland Clinic Foundation
  • , Jenny KimAffiliated withTaussig Cancer Institute - R40, Cleveland Clinic Foundation
  • , Mahrukh K. GanapathiAffiliated withTaussig Cancer Institute - R40, Cleveland Clinic Foundation
  • , Ram GanapathiAffiliated withTaussig Cancer Institute - R40, Cleveland Clinic Foundation Email author 

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access


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.


Angiogenesis Tyrosine kinase inhibitors Hypertension VEGF polymorphism Outcome Toxicity