Journal
TRENDS IN CELL BIOLOGY
Volume 26, Issue 1, Pages 52-64Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2015.07.009
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Funding
- Ovarian Cancer Research Fellowship (OCRF)
- Italian Association for Cancer Research (AIRC) Fellowships for Abroad
- National Institutes of Health (NIH) [P50CA168504, R01HL52725]
- OCRF
- Breast Cancer Research Foundation (BCRF)
- NATIONAL CANCER INSTITUTE [P50CA168504] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL052725] Funding Source: NIH RePORTER
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DNA double-strand breaks (DSBs) are cytotoxic lesions that threaten genomic integrity. Failure to repair a DSB has deleterious consequences, including genomic instability and cell death. Indeed, misrepair of DSBs can lead to inappropriate end-joining events, which commonly underlie oncogenic transformation due to chromosomal translocations. Typically, cells employ two main mechanisms to repair DSBs: homologous recombination (HR) and classical nonhomologous end joining (C-NHEJ). In addition, alternative error-prone DSB repair pathways, namely alternative end joining (alt-EJ) and single-strand annealing (SSA), have been recently shown to operate in many different conditions and to contribute to genome rearrangements and oncogenic transformation. Here, we review the mechanisms regulating DSB repair pathway choice, together with the potential interconnections between HR and the annealing-dependent error-prone DSB repair pathways.
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