Vascular endothelial growth factor pathway’s influence on bevacizumab efficacy in metastatic colorectal cancer treatment

Abstract

In this article, an article published in the World Journal of Gastrointestinal Oncology, which focuses on whether the expression of programmed death-ligand 1 (PD-L1) affects the effectiveness of chemotherapy regimens, including bevacizumab, in treating patients with colorectal cancer (CRC). Through neutralization of vascular endothelial growth factor (VEGF), bevacizumab inhibits tumor angiogenesis, impairing neovascularization and thereby depriving the tumor of essential nutrients and oxygen. Conversely, PD-L1 binding to VEGF receptor 2 promotes angiogenesis, supporting tumor vasculature. The interplay between these pathways complicates the assessment of bevacizumab’s efficacy in cancer therapy, notably in CRC, where VEGF and PD-L1 significantly affect treatment response. This review examines metastatic CRC treatment strategies, focusing on bevacizumab’s mechanism of action and the role of PD-L1 in this therapeutic context.

Keywords: Bevacizumab; Chemotherapy; Metastatic colorectal cancer; PD-1/PD-L1 axis; Therapeutic approach; Vascular endothelial growth factor

Core Tip: In the management of colorectal carcinoma, bevacizumab wields its therapeutic impact via the neutralization of vascular endothelial growth factor (VEGF), a paramount mediator of intratumoral angiogenesis. This inhibitory action on VEGF obstructs neovascularization, consequently sequestering the essential sustenance of nutrients and oxygen requisite for tumoral proliferation and viability. Contrarily, the interaction between programmed death-ligand 1 and VEGF receptor 2 catalyzes the genesis of novel vasculature that sustains and nurtures the neoplasm, thereby potentiating angiogenic processes.