Journal
DNA REPAIR
Volume 19, Issue -, Pages 169-175Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2014.03.014
Keywords
DNA double strand break; Repair pathway choice; Microhomology-mediated end joining; DNA ends; Resection; 53BP1-BRCA1
Categories
Funding
- NCI NIH HHS [P01 CA174653, R01 CA092245, R01 CA167826] Funding Source: Medline
Ask authors/readers for more resources
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. (C) 2014 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available