Genetic Changes in Head and Neck Cancer

Abstract

Head and neck squamous cell carcinoma (HNSCC) is the fifth most common cancer worldwide, with a global yearly incidence of 780,000 new cases. Common sites include the oral cavity, oropharynx, hypopharynx, nasopharynx, nasal cavity, paranasal sinus, larynx and salivary glands. Tobacco and/or alcohol consumption are the two main risk factors involved in the development of HNSCC. Despite recent advances in treatment, the long-term survival rate of patients with head and neck squamous cell carcinoma has remained at 40%. Locorregional recurrence and metastasis after conventional therapy appear to be the major contributing factors for the restricted survival of patients. The development of HNSCC is a multistep process accompanied by genetic and epigenetic changes, including loss of heterozygosity, gene inactivation by methylation and gene amplification. Different studies have revealed numerous molecular abnormalities in HNSCC, including activation of oncogenes such as EGFR, cyclin D1 and COX-2; inactivation of tumor suppressor genes such as TP53, p16, p27, and WAF1/C1P1; and expression of angiogenic and metastatic factors, as well as genetic polymorphisms of metabolic enzymes. This review presents current information about the main genetic changes involved in the development of head and neck cancer, which shows potential prognostic value and discusses some factors that contribute to the controversy concerning their prognostic importance.