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To maintain the integrity of the genome, cells have evolved a complex set of pathways that function in response to DNA damage. Components of this response include (i) cell cycle checkpoints that prevent damaged DNA from being replicated, (ii) induction of programmed cell death to prevent the transmission of potentially mutagenic genetic changes and (iii) DNA repair pathways that remove various types of DNA lesions such as single base lesions, single strand breaks (SSB)s or double strand breaks (DSB)s. DSBs are considered the most lethal form of DNA damage because, unlike almost any other types of DNA damage that have an intact undamaged template strand to guide the repair, the integrity of both strands of the duplex is lost (Khanna and Jackson, 2001). DSBs can be induced by environmental factors such as ionizing radiation, ultraviolet light, therapeutic treatment but also occur as a consequence of specific physiological processes such as DNA replication, the V(D)J recombination in B and T-lymphocytes or the immunoglobulin class switch recombination (CSR) within immunoglobulin variable domains in B-lymphocytes occurring during the development and maturation of the immune system (Ferguson and Alt, 2001, Revy et al., 2005). In order to maintain the integrity of the DNA information, cells recruit stringent DSB repair machinery to ensure the efficient repair of various types of DNA damage. Thus, failure to properly repair the DSBs may cause chromosomal abnormalities, which in turn, may lead to genomic instability and predispose the cells to malignant transformation. Moreover, the importance of DNA repair in protecting against DSB-induced genomic instability is suggested by the increased incidence of cancer in autosomal recessive DNA repair deficient human syndromes, such as BRCA1/2 deficient breast cancers (Futreal et al., 1994). Thus, since genomic instability is a common characteristic of both inherited and sporadic forms of cancer cells, it is likely that abnormalities in DNA repair contribute to the development and progression of sporadic cancers (Khanna and Jackson, 2001). DSBs can be repaired by two major pathways, homology–directed repair (HR) and nonhomologous end-joining (NHEJ) (Helleday et al., 2007). HR is active during the late S and G2 phases of the cell cycle and uses the intact sister chromatid as the template for repair

The Role of Error-Prone Alternative Non-Homologous End-Joining in Genomic Instability in Cancer