ABSTRACT
There are many DNA damaging agents which attack cellular DNA on a daily basis. These may be endogenous, such as cellular metabolic products, or exogenous such as ionizing-or ultraviolet-radiation. Exposure to such agents can lead to several types of DNA damage. The most deleterious of these is the double-strand break (DSB). DSBs, if left unrepaired, may lead to gross chromosomal rearrangements and ultimately cell death. Within the cell there are two main DSB repair pathways: non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ is predominantly used within G1 of the cell cycle, with a signifi cant contribution seen from
Department of Radiation Oncology and Molecular Biology Program, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY10065, United States. aEmail: powells@mskcc.org *Corresponding author †This work was supported by PHS grant CA107640 No confl icts of interest
HR during S/G2 when a sister chromatid becomes available for use as a template (SilvaMao et al. 2008). Due to HR utilizing a homologous template, it is typically an error-free mechanism of repair. In contrast, NHEJ involves the simple ligation of two broken ends together, without the necessity of homology and frequently with end-modifi cation, leading to a higher probability of erroneous or mutagenic repair.
