Application of Host Cell Reactivation in Evaluating the Effects of Anticancer Drugs and Environmental Toxicants on Cellular DNA Repair Activity in Head and Neck Cancer

DNA repair pathways are targets of numerous anticancer drugs including natural and chemical compounds, which direct cancer cells toward apoptosis. However, different types of cancer cells consist of various alterations in DNA repair genes that make cancer cells become drug-resistant and lead to treatment failure and disease recurrence. On the contrary, cancer cells may also possess defects in certain DNA repair pathway that make them are susceptible to certain compounds, which inhibit another DNA repair pathway inside the cancer cells. As a result, these compounds selectively kill the cancer cells and are less harmful to the normal ones. Understanding the effects of anticancer drugs on DNA repair as well as the DNA repair activity of cancer cells themselves are important for improvement of anticancer treatment. Similarly, this information is helpful for elucidation of the carcinogenicity of environmental toxicants. This chapter introduces the crosstalk between anticancer drugs, environmental toxicants and DNA repair pathways in head and neck cancer. In addition, the application of an easy, fast and measurable in vivo functional assay for nucleotide excision repair (NER) and DNA repair via homologous recombination (HR) and non-homologous end-joining (NHEJ) pathways is shown to examine the cellular DNA repair activity responding to anticancer drugs or environmental toxicants. By which the functional roles of DNA repair genes in response to anticancer treatments and genotoxic substances could be evolved in head and neck cancer cells.