Vascular endothelial growth factor (VEGF)
Tumors cannot grow without new vessel formation (angiogenesis).
The dominant growth factor controlling angiogenesis is vascular endothelial growth factors (VEGFs). The VEGFs bind to VEGF receptors (VEGFRs), tyrosine kinase receptors on the cell surface. This can be reduced by using the VEGF-blocking monoclonal antibody bevacizumab, by providing decoy receptors to reduce binding on true receptors (aflibercept), or employing the small molecule tyrosine kinase inhibitors (TKIs), such as sorafenib and sunitinib, that inhibit the enzyme in the receptor.

Epidermal growth factor (EGF)
The epidermal growth factor (EGF) proteins promote cell proliferation and differentiation by binding to the EGF receptor (EGFR), a tyrosine kinase receptor present on the cell surface. This can be blocked by the EGFR inhibitor monoclonal antibody cetuximab, or small molecules that block the tyrosine kinase enzymes (TKIs) such as gefitinib and erlotinib.

Tyrosine kinase (RTK) inhibitor
An orally bioavailable, indolinone-derived nintedanib, RTK inhibitor with potential antiangiogenic and antineoplastic activities. It selectively binds to and inhibits vascular endothelial growth factor receptor, fibroblast growth factor receptor, and platelet-derived growth factor receptor tyrosine kinases, which may result in the induction of endothelial cell apoptosis; a reduction in tumor vasculature; and the inhibition of tumor cell proliferation and migration.

Adapted from Wikipedia, the free encyclopedia. Internet. Accessed on March 3, 2017.

National Cancer Institute. NCI Drug Dictionary. Internet. Accessed on July 15, 2017.