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Genomes are continually attacked by both endogenous and exogenous agents that damage DNA. DNA damage in the form of DNA breaks can lead to chromosome translocations, cell cycle arrest, and apoptosis. Homologous recombination is an essential biological process that ensures the accurate repair of DNA breaks and thereby contributes to genomic integrity (Kuzminov 1999; Paques and Haber 1999). DNA double-strand breaks (DSBs) are considered the principal lethal DNA damage resulting from ionizing radiation and cross-linking drugs. In addition, DSB can arise from endogenous processes, such as replication fork stalling during attempted replication over a single strand-break and topoisomerase poisons that are common therapies in the treatment of human cancers (Arnaudeau, Lundin et al. 2001). It is of great importance that cells recognise DSBs and act upon them rapidly and efficiently, because cell death or impaired cell function can occur if these are left unrepaired or are repaired inaccurately. In addition to DNA repair mechanisms, cell cycle checkpoint activation processes are initiated in response to DNA damage. More specifically, DNA damage signals to arrest cell cycle progression, giving the cell more time to repair what might otherwise be a fatal lesion (Henning and Sturzbecher 2003).

DNA Damage Repair and Cancer: The Role of RAD51 Protein and Its Genetic Variants