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DNA 염기손상 치유유전자의 변이와 두경부암 발생 위험성

THE EFFECT OF GENETIC VARIATION IN THE DNA BASE REPAIR GENES ON THE RISK OF HEAD AND NECK CANCER

최병준|윤병욱|오정환
대한구강악안면외과학회 (Korean Association Of Oral And Maxillofacial Surgeons)|2008.10|대한구강악안면외과학회지 (Journal of the Korean Association of Oral and Maxillofacial Surgeons)|제34권 제5호|pp. 509-517

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참고문헌

주제분류치의학

초록

Abstract

DNA damage accumulates in cells as a result of exposure to exogenous agents such as benzopyrene, cigarette smoke, ultraviolet light, X-ray, and endogenous chemicals including reactive oxygen species produced from normal metabolic byproducts. DNA damage can also occur during aberrant DNA processing reactions such as DNA replication, recombination, and repair. The major of DNA damage affects the primary structure of the double helix; that is, the bases are chemically modified. These modification can disrupt the molecules’ regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. DNA repair genes and proteins scan the global genome to detect and remove DNA damage and damage to single nucleotides. Direct reversal of DNA damage, base excision repair, double strand break. DNA repair are known relevant DNA repair mechanisms. Four different mechanisms are distinguished within excision repair: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Genetic variation in DNA repair genes can modulate DNA repair capacity and alter cancer risk. The instability of a cell to properly regulate its proliferation in the presence of DNA damage increase risk of gene mutation and carcinogenesis. This article aimed to review mechanism of excision repair and to understand the relationship between genetic variation of excision repair genes and head and neck cancer.

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