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DNA Repair (Amst). 2014 Jul;19:169-75. doi: 10.1016/j.dnarep.2014.03.014. Epub 2014 Apr 18.

DNA double-strand break repair pathway choice and cancer.

Author information

1
Institute for Cancer Genetics & Department of Genetics and Development, Columbia University Medical Center, New York, NY, USA.
2
Institute for Cancer Genetics & Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, USA.
3
Institute for Cancer Genetics & Department of Genetics and Development, Columbia University Medical Center, New York, NY, USA. Electronic address: jg130@columbia.edu.

Abstract

Since DNA double-strand breaks (DSBs) contribute to the genomic instability that drives cancer development, DSB repair pathways serve as important mechanisms for tumor suppression. Thus, genetic lesions, such as BRCA1 and BRCA2 mutations, that disrupt DSB repair are often associated with cancer susceptibility. In addition, recent evidence suggests that DSB "mis-repair", in which DSBs are resolved by an inappropriate repair pathway, can also promote genomic instability and presumably tumorigenesis. This notion has gained currency from recent cancer genome sequencing studies which have uncovered numerous chromosomal rearrangements harboring pathological DNA repair signatures. In this perspective, we discuss the factors that regulate DSB repair pathway choice and their consequences for genome stability and cancer.

KEYWORDS:

53BP1–BRCA1; DNA double strand break; DNA ends; Microhomology-mediated end joining; Repair pathway choice; Resection

PMID:
24746645
PMCID:
PMC4051845
DOI:
10.1016/j.dnarep.2014.03.014
[Indexed for MEDLINE]
Free PMC Article

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