Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8222448 | International Journal of Radiation Oncology*Biology*Physics | 2013 | 10 Pages |
Abstract
DNA damage can occur as a result of endogenous metabolic reactions and replication stress or from exogenous sources such as radiation therapy and chemotherapy. DNA double strand breaks are the most cytotoxic form of DNA damage, and defects in their repair can result in genome instability, a hallmark of cancer. The major pathway for the repair of ionizing radiation-induced DSBs in human cells is nonhomologous end joining. Here we review recent advances on the mechanism of nonhomologous end joining, as well as new findings on its component proteins and regulation.
Related Topics
Physical Sciences and Engineering
Physics and Astronomy
Radiation
Authors
Chen PhD, Susan P. PhD,