Epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR) (EGFR/VEGFR)

The combined inhibition of the Epidermal Growth Factor Receptor (EGFR) and angiogenic Receptor Tyrosine Kinases (RTKs), such as Vascular Endothelial Growth Factor Receptor (VEGFR), represents a strategic approach to treating Non-Small Cell Lung Cancer (NSCLC) (Source: PubMed, PMID: 31593850). EGFR is a transmembrane glycoprotein that regulates cell proliferation and survival, and its mutation is a major driver in NSCLC (Source: UniProt, P00533). Angiogenic RTKs like VEGFR2 are critical for tumor neovascularization, providing the blood supply necessary for tumor expansion (Source: UniProt, P35968). Research indicates significant crosstalk between these pathways, where EGFR signaling upregulates VEGF expression, and VEGF signaling can mediate resistance to EGFR inhibitors (Source: Journal of Thoracic Oncology, 2020). Therapeutic strategies include multi-targeted tyrosine kinase inhibitors like vandetanib or combination therapies such as erlotinib with bevacizumab (Source: FDA, 2021). This dual targeting aims to overcome bypass resistance mechanisms and improve progression-free survival in patients with advanced disease (Source: Lancet Oncology, 2019). Common adverse effects associated with this dual blockade include hypertension and skin toxicity, reflecting the physiological roles of these receptors in vascular and epithelial homeostasis (Source: Nature Reviews Clinical Oncology, 2018).

Other names

EGFR/VEGFR dual inhibitionEGFR and angiogenic RTK co-inhibitionEGFR-VEGF axisCombined EGFR and VEGFR targeting

Simultaneous inhibition of the EGFR signaling pathway, which drives tumor cell proliferation and survival, and the VEGFR/angiogenic pathways, which facilitate tumor neovascularization and nutrient supply.