Pathways and genes of DNA double-strand break repair associated with head and neck cancer.
- Author:
Jung Hwan OH
1
;
Deok Won LEE
;
Dong Mok RYU
Author Information
1. Department of Oral and Maxillofacial Surgery, School of Dentistry, Kyung-Hee University, Korea.
- Publication Type:Review
- Keywords:
DNA double-strand breaks(DSBs);
Homologous recombination(HR);
Non-homologous end-joining(NHEJ);
Cancer
- MeSH:
Aging, Premature;
Cell Death;
Chromatids;
DNA;
DNA Damage;
Genomic Instability;
Hand;
Head;
Head and Neck Neoplasms;
Humans;
Loss of Heterozygosity;
Oxygen;
Radiation, Ionizing;
Siblings
- From:Journal of the Korean Association of Oral and Maxillofacial Surgeons
2009;35(1):1-6
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
DNA double-strand breaks (DSBs) occur commonly in the all living and in cycling cells. They constitute one of the most severe form of DNA damage, because they affect both strand of DNA. DSBs result in cell death or a genetic alterations including deletion, loss of heterozygosity, translocation, and chromosome loss. DSBs arise from endogenous sources like metabolic products and reactive oxygen, and also exogenous factors like ionizing radiation. Defective DNA DSBs can lead to toxicity and large scale sequence rearrangement that can cause cancer and promote premature aging. There are two major pathways for their repair: homologous recombination(HR) and non-homologous end-joining(NHEJ). The HR pathway is a known "error-free" repair mechanism, in which a homologous sister chromatid serves as a template. NHEJ, on the other hand, is a "error-prone" pathway, in which the two termini of the broken DNA molecule are used to form compatible ends that are directly ligated. This review aims to provide a fundamental understanding of how HR and NHEJ pathways operate, cause genome instability, and what kind of genes during the pathways are associated with head and neck cancer.
