ABSTRACT
DNA repair is a complicated biological process that maintains genome stability (Wood et al. 2001). Exposure to environmental carcinogens, such as tobacco smoke and ultraviolet (UV) radiation, can result in various types of DNA damage (Phillips 2002; Stokes and Comb 2008) that promote the development of diseases, including cancer. During evolution, most species have developed the necessary spectrum of DNA repair machinery to battle genomic insults from environmental hazards and maintain genomic integrity (Hoeijmakers 2001) (see Chapter 1). To date, more than 165 human DNA repair genes have been identifi ed that can be categorized into several distinct pathways: base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), and double-strand break repair (DSBR) (Wood et al. 2005; Wood 2011).
