Abstract
Mammalian cells are constantly exposed to endogenous and exogenous genotoxic agents, and distinct repair pathways have evolved to handle the different types of DNA damage. The six major repair pathways are base excision repair (BER), direct reversal of damage, mismatch excision repair (MMR), nucleotide excision repair (NER), homologous recombination (HR), and nonhomologous end-joining (NHEJ). Over 130 human DNA repair genes have been reported, and more will be identified. Many single-nucleotide polymorphisms (SNPs) of DNA repair genes have also been reported and some of them may affect DNA repair functions. Although, on an individual basis, SNPs may cause only small changes in repair activity, their presence at polymorphic frequencies in the human population may contribute to a high proportion of cancer cases and the variation of interindividual responses to cancer therapies.