Effective targeting of the epidermal growth factor receptor (EGFR) for treating oral cancer: a promising approach

• Published in: Anticancer research 2014-04, Vol.34 (4), p.1547-1552
• Main Authors: Ribeiro, Flávia Andressa Pidone, Noguti, Juliana, Oshima, Celina Tizuko Fujiyama, Ribeiro, Daniel Araki
• Format: Article
• Language: English
• Subjects: Antineoplastic Agents - pharmacology; Antineoplastic Agents - therapeutic use; Humans; Molecular Targeted Therapy; Mouth Neoplasms - drug therapy; Mouth Neoplasms - genetics; Mouth Neoplasms - metabolism; Mutation; Polymorphism, Genetic; Receptor, Epidermal Growth Factor - antagonists & inhibitors; Receptor, Epidermal Growth Factor - genetics; Receptor, Epidermal Growth Factor - metabolism; Signal Transduction - drug effects
• ISSN: 1791-7530

Oral cancer is a serious problem growing in incidence in many parts of the world; it is considered the sixth most common cancer and despite sophisticated surgical and radiotherapeutic modalities, oral squamous cell carcinoma, which represents 90% of oral cancers, is characterized by poor prognosis and a low survival rate. The Epidermal growth factor receptor family of receptor tyrosine kinases (RTK) comprises of four distinct receptors: the EGFR (also known as ErbB-1/HER1), ErbB-2 (neu, HER2), ErbB-3 (HER3) and ErbB-4 (HER4). Several studies have been published on the role of EGFR in the pathogenesis of oral carcinoma. The aim of the present review is to describe the role of EGFR pathway in oral cancer with special focus on its role during the carcinogenesis process as a result of therapeutic approaches of EGFR in oral cancer. The EGFR is a 170-kDa cell-surface protein involved in many biological processes, such as proliferation, migration, DNA synthesis and adhesion. Overexpression of EGFR results in a poor prognosis in oral cancer and its activation is associated with the malignant phenotype, inhibition of apoptosis and increased metastatic potential. EGFR variations and mutations have been correlated with tumor formation, and possibly alter the therapeutic efficacy of EGFR inhibitors.