DNA 이중나선파손의 수복 과정과 이와 연관된 두경부암 발생 유전자

• 영문명: PATHWAYS AND GENES OF DNA DOUBLE-STRAND BREAK REPAIR ASSOCIATED WITH HEAD AND NECK CANCER
• 발행기관: 대한구강악안면외과학회
• 저자명: 오정환(Jung-Hwan Oh) 이덕원(Deok-Won Lee) 류동목(Dong-Mok Ryu)
• 간행물 정보: 『대한구강악안면외과학회지』대한구강악안면회과학회지 제35권 제1호, 1~6쪽, 전체 6쪽
• 주제분류: 의약학 > 내과학
• 파일형태: PDF
• 발행일자: 2009.02.28

영문 초록

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.

키워드

DNA double-strand breaks(DSBs) Homologous recombination(HR) Non-homologous end-joining(NHEJ) Cancer