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The Role of HGF/c-MET in Head and Neck Squamous Cell Carcinoma
Book chapter

The Role of HGF/c-MET in Head and Neck Squamous Cell Carcinoma

Tanguy Y. Seiwert, Tim N. Beck and Ravi Salgia
Molecular Determinants of Head and Neck Cancer, pp 91-111
09 Apr 2014

Abstract

c-MET EGFR Head and neck cancer HER HGF HGFR Receptor tyrosine kinases Squamous cell cancer Targeted therapy
Head and Neck Squamous Cell Carcinoma (HNSCC) remains a formidable challenge to physicians, scientists, and patients. New targets that can be exploited to improve the outcome of patients afflicted with this dreadful disease are desperately needed: one such potential target is c-MET. The c-MET receptor tyrosine kinase, also known as hepatocyte growth factor receptor (HGFR), is robustly overexpressed and sometimes mutated or amplified in head and neck cancer cells, while overexpression of its ligand, hepatocyte growth factor/scatter factor (HGF/SF), often occurs in tumor-adjacent mesenchymal cells, providing paracrine signals that support tumor growth. Activation of c-MET stimulates numerous downstream signaling pathways that contribute to tumor growth, including GRB2/RAS, PI3K, STAT3, SRC, β-catenin, and Notch. Overexpression or anomalous activation of c-MET is often associated with resistance to targeted therapies inhibiting receptor tyrosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR), that communicate to similar growth factor cascades. In this review, we emphasize the role of c-MET/HGF in HNSCC as well as the potential for therapeutic targeting of this receptor.

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Collaboration types
Domestic collaboration
Web of Science research areas
Oncology
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