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Targeting Tumor Angiogenesis in HNSCC: The Role of VEGF Inhibitors and Combination Therapies

J. Narayanan1*, R. Sridevi1, V. Chitra1, V. Manimaran2, K. Manikandan3

1Department of Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, India

2Department of Pharmaceutics, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, India

3Department of Pharmaceutical Analysis, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, India

*For Correspondence

narayanj@srmist.edu.in 

Publication Date: June 30, 2025
DOI: 10.5281/zenodo.14830074
Read Abstract

Abnormalities in the vasculature of tumors, including undeveloped structure, increased permeability, and a disorganized microenvironment, are important characteristics of cancer. The problems are caused by malfunctioning endothelium and mural cellular structures, in addition to disrupted connections with the extracellular matrix (ECM). Tumor endothelial cells (TECs) derived from cancer stem cells undergo detachment, resulting in an elevation of vascular permeability and promoting the dissemination of the tumor. Pericyte detachment exacerbates these issues by augmenting mechanical strain and interrupting blood circulation, resulting in a hypoxic, acidic environment that promotes tumor proliferation and the production of ascites. Increased levels of Vascular Endothelial Growth Factor (VEGF) promote angiogenesis, which are abnormal in structure and limit the efficient delivery of drugs. Tumors can also employ vasculogenic mimicry, which involves the formation of vascular systems resembling those found in embryos, in order to get food. VEGF and its related proteins (VEGF-A, VEGF-C, VEGF-D) play a crucial function in facilitating the development of new blood vessels in Head and Neck Squamous Cell Carcinoma (HNSCC). Anti-VEGF therapies, comprising monoclonal antibodies and small molecule inhibitors, offer potential benefits but face challenges associated with resistance. Inhibiting VEGF receptors with tyrosine kinase inhibitors (TKIs) can enhance advancement survival without complications and response rates, particularly when combined with immune checkpoint inhibitors (ICIs). Currently, there is ongoing research on FDA-approved tyrosine kinase inhibitors (TKIs) such as sunitinib, sorafenib, and lenvatinib, in addition to novel medicines like zanzalintinib. Future research endeavors to augment medicines that target VEGF, incorporate immunotherapy, and identify biomarkers to boost treatment outcomes for HNSCC. 

Keywords

Tumor Angiogenesis, Vascular Endothelial Growth Factor (VEGF) Pathway, Head and Neck Squamous Cell Carcinoma (HNSCC), Tyrosine Kinase Inhibitors (TKIs), Tumor Microenvironment

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