Abstract DNA double strand breakage（ DSB） is the most significantly biological effect when cells are exposed to ionizing radiation（ IR） which may result in apoptosis， checkpoint arrest， cellular senescence and DSB repair. DNA damage response（ DDR） is activated with induction of DNA damage. The mechanisms involved in DSB repair include homologous recombination（ HR） and non-homologous end-joining（ NHEJ）. HR， a template-dependent and mostly error-free pathway， plays a crucial role in protecting genome fidelity from DSB. It can be divided into three phases including presynaptic， synaptic and postsynaptic phases. For the repair of DSBs caused by IR， HR is mainly restricted in G2 and S phases while NHEJ and HR function complementarily. HR is related to the risk of tumorigenesis， predicts the survival of several kinds of carcinoma and is a novel target of cancer therapy. This article has comprehensively reviewed
the progress in understanding of the mechanism of HR repair， its associated factors affecting the fidelity in DSB repair， the concept of synthetic lethality and its association with NHEJ repair. The potential of its clinical application by targeting specific DSB repair pathways is further explored.
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