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1

Genetic polymorphisms of the DNA repair gene MPG may be associated with susceptibility to rheumatoid arthritis

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Chen S. Y., Wan L., Huang C. M., Huang Y. C., Sheu J. J. C., Lin Y. J., Liu S. P., Lan Y. C., Lai C. H., Lin C. W., Tsai C. H., Tsai F. J.
Journal of Applied Genetics
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2010
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tom 51
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nr 4
Rheumatoid arthritis (RA) is a chronic autoimmune disease and can lead to deformities and severe disabilities, due to irreversible damage of tendons, joints, and bones. A previous study indicated that a DNA repair system was involved in the development of RA. In this study, we investigated the association of four N-methylpurine-DNA glycosylase (MPG) gene polymorphisms (rs3176364, rs710079, rs2858056, and rs2541632) with susceptibility to RA in 384 Taiwanese individuals (192 RA patients and 192 control subjects). Our data show a statistically significant difference in genotype frequency distributions at rs710079 and rs2858056 SNPs between RA patients and control groups (P = 0.040 and 0.029, respectively). Our data also indicated that individuals with the GG genotype at rs2858056 SNP may have a higher risk of developing RA. In addition, compared with the haplotype frequencies between case and control groups, individuals with the GCGC haplotype appeared to be at a greater risk of RA progression (P = 0.003, OR = 1.75; 95% CI = 1.20-1.55). Our results suggest that rs710079 and rs2858056 polymorphisms and the GCGC haplotype in the MPG gene are associated with the risk of RA progression, and thus may be used as molecular markers of RA if they are confirmed by further research.
2

Bacterial DNA repair genes and their eukaryotic homologues: 5. The role of recombination in DNA repair and genome stability

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Nowosielska A.
Acta Biochimica Polonica
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2007
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tom 54
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nr 3
Recombinational repair is a well conserved DNA repair mechanism present in all living organisms. Repair by homologous recombination is generally accurate as it uses undamaged homologous DNA molecule as a repair template. In Escherichia coli homologous recombination repairs both the double-strand breaks and single-strand gaps in DNA. DNA double-strand breaks (DSB) can be induced upon exposure to exogenous sources such as ionizing radiation or endogenous DNA-damaging agents including reactive oxygen species (ROS) as well as during natural biological processes like conjugation. However, the bulk of double strand breaks are formed during replication fork collapse encountering an unrepaired single strand gap in DNA. Under such circumstances DNA replication on the damaged template can be resumed only if supported by homologous recombination. This functional cooperation of homologous recombination with replication machinery enables successful completion of genome duplication and faithful transmission of genetic material to a daughter cell. In eukaryotes, homologous recombination is also involved in essential biological processes such as preservation of genome integrity, DNA damage checkpoint activation, DNA damage repair, DNA replication, mating type switching, transposition, immune system development and meiosis. When unregulated, recombination can lead to genome instability and carcinogenesis.
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Bacterial DNA repair genes and their eukaryotic homologues: 3. AlkB dioxygenase and Ada methyltransferase in the direct repair of alkylated DNA

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Nieminuszczy J., Grzesiuk E.
Acta Biochimica Polonica
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2007
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tom 54
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nr 3
Environmental and endogenous alkylating agents generate cytotoxic and mutagenic lesions in DNA. Exposure of prokaryotic cells to sublethal doses of DNA alkylating agents induces so called adaptive response (Ada response) involving the expression of a set of genes which allows the cells to tolerate the toxic and mutagenic action of such agents. The Ada response includes the expression of four genes: ada, alkA, alkB, and aidB. The product of ada gene, Ada protein, is an activator of transcription of all four genes. DNA bases damaged by alkylation are removed by distinct strategies. The most toxic lesion 3meA is removed by specific DNA glycosylase initiating base excising repair. The toxic and mutagenic O6meG is repaired directly by methyltransferases. 1meA and 3meC are corrected by AlkB DNA dioxygenase. The mechanisms of action of E. coli AlkB dioxygenase and its human homologs ABH2 and ABH3 are described in more details.
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Searching for in vitro biomarkers of susceptibility to prostate and cervical cancers by analysis of chromosomal instability, gamma-H2AX foci, polymorphisms in DNA repair genes and apoptosis

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Wegierek-Ciuk A., Arabski M., Kedzierawski P., Florek A., Solowiej D., Gozdz S., Lisowska H., Kowalik A., Kowalska M., Wojcik A., Polanska J., Lankoff A.
Journal of Pre-Clinical and Clinical Research
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2015
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tom 09
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nr 2
Introduction and objective. According to the cancer epidemiology databases, cancer is the second leading cause of death in developing countries. Moreover, the WHO predicts a continuing increase in the incidence of cancer, extending this trend well into the next several decades. Hence, it seems obvious that the prediction of cancer susceptibility and early diagnosis is an important goal for modern biomedical sciences. The aim of this study is to clarify the value of chromosomal damage, capacity for the repair of double-strand breaks (DSBs), polymorphisms in DNA repair genes, and apoptosis as prognostic markers for prostate and cervical cancer. Materials and methods. 30 prostate cancer patients and 30 cervical cancer patients were enrolled into the study. In addition, 30 healthy female donors and 30 healthy male donors served as controls. The following endpoints were investigated: frequency of micronuclei, gamma-H2AX fluorescence, XRCC1 194C>T, XRCC1 399G>A, XRCC3 IVS5–14 A>G, OGG1 326 Ser>Cys polymorphisms and apoptosis. Results. Among all tested factors, only the homozygous variant (Arg/Arg) in XRCC1 (399 Arg/Gln) was strongly associated with prostate cancer risk, and only a low apoptotic response was connected with cervical cancer risk. The presented study confirmed a positive association between the frequency of MN and increased prostate and cervical cancer risk. However, such a biomarker is not cancer specific. In addition, the information gained by analyzing the gamma-H2AX fluorescence, as well apoptosis, had no value for predicting the risk of prostate and cervical cancers. Conclusions. The final conclusion of the study is that cancer susceptibility is a complex phenotype not readily detectable in relatively small studies by functional assays or analysis of SNP in few, selected genes.
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Bacterial DNA repair genes and their aukaryotic homologues: 1. Mutations in genes involved in base excision repair [BER] and DNA-end processors and their implication in mutagenesis and human disease

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Krwawicz J., Arczewska K. D., Speina E., Maciejewska A., Grzesiuk E.
Acta Biochimica Polonica
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2007
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tom 54
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nr 3
Base excision repair (BER) pathway executed by a complex network of proteins is the major system responsible for the removal of damaged DNA bases and repair of DNA single strand breaks (SSBs) generated by environmental agents, such as certain cancer therapies, or arising spontaneously during cellular metabolism. Both modified DNA bases and SSBs with ends other than 3'-OH and 5'-P are repaired either by replacement of a single or of more nucleotides in the processes called short-patch BER (SP-BER) or long-patch BER (LP-BER), respectively. In contrast to Escherichia coli cells, in human ones, the two BER sub-pathways are operated by different sets of proteins. In this review the selection between SP- and LP-BER and mutations in BER and end-processors genes and their contribution to bacterial mutagenesis and human diseases are considered.
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Bacterial DNA repair genes and their eukaryotic homologues: 2. Role of bacterial mutator gene homologues in human disease. Overview of nucleotide pool sanitization and mismatch repair system

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Arczewska K. D., Kusmierek J. T.
Acta Biochimica Polonica
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2007
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tom 54
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nr 3
Since the discovery of the first E. coli mutator gene, mutT, most of the mutations inducing elevated spontaneous mutation rates could be clearly attributed to defects in DNA repair. MutT turned out to be a pyrophosphohydrolase hydrolyzing 8-oxodGTP, thus preventing its incorporation into DNA and suppresing the occurrence of spontaneous AT→CG transversions. Most of the bacterial mutator genes appeared to be evolutionarily conserved, and scientists were continuously searching for contribution of DNA repair deficiency in human diseases, especially carcinogenesis. Yet a human MutT homologue - hMTH1 protein - was found to be overexpressed rather than inactivated in many human diseases, including cancer. The interest in DNA repair contribution to human diseases exploded with the observation that germline mutations in mismatch repair (MMR) genes predispose to hereditary non-polyposis colorectal cancer (HNPCC). Despite our continuously growing knowledge about DNA repair we still do not fully understand how the mutator phenotype contributes to specific forms of human diseases.
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