Journal
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
Volume 806, Issue -, Pages 64-74Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.mrfmmm.2017.07.008
Keywords
DNA damage; DNA repair; Genome instability; Radiation
Funding
- National Institutes of Health [R01 GM084020]
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DNA damage is a constant threat to genome integrity. DNA repair and damage signaling networks play a central role maintaining genome stability, suppressing tumorigenesis, and determining tumor response to common cancer chemotherapeutic agents and radiotherapy. DNA double-strand breaks (DSBs) are critical lesions induced by ionizing radiation and when replication forks encounter damage. DSBs can result in mutations and large-scale genome rearrangements reflecting mis-repair by non-homologous end joining or homologous recombination. Ionizing radiation induces genetic change immediately, and it also triggers delayed events weeks or even years after exposure, long after the initial damage has been repaired or diluted through cell division. This review covers DNA damage signaling and repair pathways and cell fate following genotoxic insult, including immediate and delayed genome instability and cell survival/cell death pathways.
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