DNA Double-Strand Break Repair and Its Clinical Implications

Dear Colleagues,
DNA double-strand break (DSB), arising from exogenous and endogenous stresses or cellular programmed activities, is the most lethal DNA lesion in cells, since unrepaired or incorrectly repaired DSB results in genome instability, cellular senescence or cell death, which further promotes tumorigenesis, genetic disorders and neurodegenerative diseases. After several decades’ study, at least four pathways have been discovered in mammalian cells to deal with this type of DNA lesion, including two major pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), as well as two minor pathways, microhomology-mediated end joining (MMEJ) and single-strand annealing (SSA). Although HR and NHEJ have been extensively studied, many new important players and regulatory mechanisms are still being discovered, filling the gap in understanding the cellular process. Recently, the important roles for MMEJ and SSA in tumorigenesis and clinical application are attracting more and more attention, but it has to be noted that the knowledge of these two pathways are quite limited. For an example, the major players in these two processes have not been clearly defined. In addition, it is also of importance to understand mechanisms how cells pick up a right pathway to repair DSB. Usually, HR is a high fidelity DSB repair pathway because it utilizes intact sister chromatin DNA as template to repair broken one. Whereas, another three are error-prone, especially MMEJ and SSA, which are instinctively mutagenic since large deletions or insertions often occur during repair. Therefore, tight regulation of pathway choice for DSB repair is required to maintain genome stability and cell health. Moreover, understanding molecular mechanisms of DSB repair and pathway choice also strongly promotes development of drug or therapeutic approaches in cancer therapy, especially for personalized therapy. 
This Special Issue calls for papers that focus on mechanisms of DSB repair and pathway choice, biological consequences caused by DSB repair deficiency, and clinical implications. 
We look forward to your participation. 

Dr. Huiming Lu
Guest Editor

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• DNA double-strand break
• pathway choice
• homologous recombination
• non-homologous end joining
• microhomology-mediated end joining
• single-strand annealing
• premature aging
• tumorigenesis
• neurodegeneration