Increased DNA Damage and Decreased DNA Repair Following Poly(ADP‐ribose) Glycohydrolase Inhibition and Chemotherapy
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چکیده
منابع مشابه
OGG1 DNA Repair Gene Polymorphism As a Biomarker of Oxidative and Genotoxic DNA Damage
Background: Single nucleotide polymorphisms in 8-oxoguanine DNA glycosylase-1 (OGG1) gene modulates DNA repair capacity and functions as one of the first lines of protective mechanisms against 8-hydroxy-2’-deoxyguanosine (8-OHdG) mutagenicity. OGG1-Cys326 gene polymorphism may decrease DNA repair function, causing oxidative stress due to higher oxidative DNA damage. The main purpose of this stu...
متن کاملDNA Damage, Mutagenesis, and DNA Repair
This special issue of the Journal of Nucleic Acids is dedicated to DNA damage and two important biological consequences provoked by such damage: lesion repair and lesion-induced mutagenesis. These phenomena have attracted broad interest among a large community of scientists that cross disciplines frommathematics, physics, chemistry, and biology to clinical scientists. The importance of DNA dama...
متن کاملDNA Damage, DNA Repair and Cancer
DNA damage is a change in the basic structure of DNA that is not itself replicated when the DNA is replicated. A DNA damage can be a chemical addition or disruption to a base of DNA (creating an abnormal nucleotide or nucleotide fragment) or a break in one or both chains of the DNA strands. When DNA carrying a damaged base is replicated, an incorrect base can often be inserted opposite the site...
متن کاملDNA damage, DNA repair and disease
Damage to cellular DNA can result in the loss of genetic information, in cellcycle arrest or even in cell death. So DNA is constantly surveyed for the presence of lesions and appropriate responses are mounted: failure can lead to genomic instability, mutations and ultimately cancer. In the last few years, rapid progress has been made in understanding many aspects of DNA repair. For example, it ...
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ژورنال
عنوان ژورنال: The FASEB Journal
سال: 2010
ISSN: 0892-6638,1530-6860
DOI: 10.1096/fasebj.24.1_supplement.878.3