The VEGF rise in blood of bevacizumab patients is not based on tumor escape but a host-blockade of VEGF clearance.

ABSTRACT: Vascular endothelial growth factor (VEGF) has become a major target in cancer treatment as it promotes tumor angiogenesis. Therapy with anti-VEGF antibody bevacizumab reportedly induces high levels of circulating VEGF which may potentially contribute to resistance. Based on animal or computational models, mechanisms of VEGF induction by bevacizumab have been proposed but not verified in the clinical setting. Hence, we evaluated sixty patients with colorectal cancer metastases for changes in plasma VEGF during neoadjuvant/conversion and adjuvant chemotherapy with or without bevacizumab. VEGF expression was assessed in tissue sections of liver metastases. The VEGF source was investigated with in vitro cultures of tumor, endothelial cells, fibroblasts and platelets, and potential protein stab

SUBMITTER: Alidzanovic L 

PROVIDER: S-EPMC5302983 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature