Aashish Soni

TL;DR: Homologous recombination repair and alternative NHEJ show strong cell-cycle dependency and are likely to benefit from radiation therapy mediated redistribution of tumor cells throughout the cell- cycle, making HRR a particularly intriguing target for treatments aiming to improve the efficacy of radiation therapy.

TL;DR: A state-of-the-art review of the molecular underpinnings of repair pathways that process DSBs in higher eukaryotes, their strengths and limitations, as well as aspects of repair pathway choice and hierarchy are provided.

TL;DR: A functional hierarchy among DSB processing pathways is proposed that makes alt-EJ the global backup pathway and possible ramifications in cellular DSB management and pathway choice, and its implications in radiation carcinogenesis and the design of novel therapeutic approaches are discussed.

TL;DR: The results identify Parp-1 and Lig1 and 3 as factors involved in translocation formation and show that Xrcc1 reinforces the function of Lig3 in the process without being required for it, which has implications for the mechanism of action of Parp inhibitors.

TL;DR: It is shown that chromatin destabilization by clusters of DNA double-strand-breaks (DSBs) generated by the I-SceI meganuclease at multiple, appropriately engineered genomic sites, compromises c-NHEJ and markedly increases cell killing and translocation-formation compared to single-DSBs.