Fig. 2

Downstream molecules and effects following DNA damage due to ionizing radiation. Ionizing radiation causes damage to DNA both directly and indirectly. Indirect damage occurs through the radiation-associated formation of free radicals. Double-stranded breaks (DSBs) are the most common form of DNA damage associated with ionizing radiation. After DSBs are generated, a cascade of enzymatic processes is triggered to allow for DNA repair or to induce apoptosis. This process includes the activation of p53 and the induction of cell cycle arrest. If the damage exceeds the cell’s ability to repair itself, either apoptosis or necrosis will occur. Alternatively, there are two common mechanisms of DSB repair: Non-homologous end joining and homologous recombination. In homologous recombination, the enzymes BRCA 1 and BRCA 2 are activated and initiate repair. If repair is successful, the cell cycle can resume. If homologous recombination is unsuccessful the cell will likely undergo apoptosis. Importantly, failure of these processes in the setting of significant mutations in cell cycle regulation or the apoptotic pathway can lead to carcinogenic transformation. In non-homologous end joining, as the name suggests, non-homologous ends are joined together to mitigate DNA damage. This can lead to significant mutations in cell cycle regulation and result in carcinogenic transformation