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Human epidermal growth factor receptor 3 in head and neck squamous cell carcinomas
Author(s) -
Rysman Bénédicte,
Mouawad François,
Gros Abigaëlle,
Lansiaux Amélie,
Chevalier Dominique,
Meignan Samuel
Publication year - 2016
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.24367
Subject(s) - cetuximab , epidermal growth factor receptor , cancer research , head and neck squamous cell carcinoma , growth factor receptor , epidermal growth factor , tyrosine kinase , protein kinase b , biology , receptor tyrosine kinase , signal transduction , pi3k/akt/mtor pathway , carcinogenesis , medicine , receptor , cancer , head and neck cancer , microbiology and biotechnology , colorectal cancer
Human epidermal growth factor receptor 3 (HER3) is a member of the human epidermal growth factor receptor (HER) family. The main characteristic of HER3 is that it does not possess tyrosine kinase activity, unlike other HERs. The role of HER3 in tumorigenesis has now been recognized, particularly in head and neck squamous cell carcinomas (HNSCCs). Despite conflicting studies, HER3 was found to be overexpressed in HNSCC samples, and correlates with disease progression and poor survival, especially when it is coexpressed with other HERs. HER3 is a significant factor in HNSCC treatment resistance. Indeed, HER3 is a major mechanism described for cetuximab resistance because of modification of epidermal growth factor receptor (EGFR) internalization and by phosphotidylinositol‐3‐kinase (PI3K)/AKT signaling pathway activation. HER3 also affects resistance to tyrosine kinase inhibitors (TKIs) and thereby promotes treatment escape and radiotherapy resistance by activation of the survival signaling pathway. To counteract this, pharmacologic inhibitors of HER3 are currently in development and could significantly improve HNSCC treatment. © 2016 Wiley Periodicals, Inc. Head Neck 38 : E2412–E2418, 2016