Head and neck cancers

Head and neck cancers, also known as cancers of the upper aerodigestive tract, are chiefly squamous cell carcinomas arising in the oral cavity, pharynx, or larynx. About 40,000 persons are diagnosed with squamous cell carcinoma of the head and neck (SCCHN) in the United States each year, and about 12,000 die of the disease (1). The male:female ratio of patients is about 2:1 for oral and pharyngeal cancer but 4:1 for laryngeal cancer. Only a fraction of individuals exposed to tobacco smoke and=or alcohol develop SCCHN, suggesting that there are differences in individual susceptibility to carcinogenesis and that the impact of gene-environment interactions should be considered. Tobacco carcinogens undergo a series of metabolic activation and detoxification steps that determine the internal dose of exposure and ultimately impact the level of DNA damage incurred. Both endogenous and exogenous exposure to carcinogens or genotoxic agents cause cell-cycle delays (2) that allow cells to repair such DNA damage. Therefore, the cellular DNA repair capacity (DRC) is central to maintaining genomic integrity and normal cellular functions (3). Recently, molecular epidemiological studies of tobacco-induced carcinogenesis were comprehensively reviewed (4-6). Also, studies have shown that polymorphisms of genes that control drug metabolism (7-9) and DNA repair (10-13) may contribute to the variation in tobacco-induced carcinogenesis in the general population. This chapter focuses on recent molecular epidemiological studies with an emphasis on the role of DNA repair in susceptibility to SCCHN.

Duke Scholars

Author Qingyi Wei Population Health Sciences