Many of Double Strand Break Repair (DSBR) proteins accumulate in the vicinity of the break site, forming so-called radiation-induced foci that can be visualized by immunofluorescence or live-cell imaging methods. The timing and type of proteins recruited to the DSB defines the downstream functions of DDR pathways which range from signaling to DSB repair, cell cycle arrest or apoptosis. This differential protein recruitment thus decides the fate of a cell following DSB. We are trying to identify the novel proteins recruited at the site of DSB by IP/ChIP and MS based methods and their role in DSB repair. We are also investigating the kinetics of recruitment of these proteins as well as pathway preferences (HR or NHEJ) in sensitive and resistant leukemic cells.