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Journal articles on the topic 'Bulky DNA adduct'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Kemp, Michael G., Laura A. Lindsey-Boltz, and Aziz Sancar. "The DNA Damage Response Kinases DNA-dependent Protein Kinase (DNA-PK) and Ataxia Telangiectasia Mutated (ATM) Are Stimulated by Bulky Adduct-containing DNA." Journal of Biological Chemistry 286, no. 22 (2011): 19237–46. http://dx.doi.org/10.1074/jbc.m111.235036.

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A variety of environmental, carcinogenic, and chemotherapeutic agents form bulky lesions on DNA that activate DNA damage checkpoint signaling pathways in human cells. To identify the mechanisms by which bulky DNA adducts induce damage signaling, we developed an in vitro assay using mammalian cell nuclear extract and plasmid DNA containing bulky adducts formed by N-acetoxy-2-acetylaminofluorene or benzo(a)pyrene diol epoxide. Using this cell-free system together with a variety of pharmacological, genetic, and biochemical approaches, we identified the DNA damage response kinases DNA-dependent pr

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2

Jha, Vikash, та Hong Ling. "Structural basis for error-free bypass of bulky adduct by DNA polymerase Polκ". Acta Crystallographica Section A Foundations and Advances 70, a1 (2014): C1401. http://dx.doi.org/10.1107/s2053273314085982.

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Humans are frequently exposed to the environmentally ubiquitous and potentially carcinigenic polycyclic aromatic hydrocarbon, benzo[a]pyrene (BP). BP is metabolized to highly reactive benzo[a]pyrene diol epoxides (BPDEs) in the cells. BPDEs react with DNA predominantly at the N2 position of guanine and form bulky adducts. The major BP adduct is (+)-trans-anti-[BP]-N2-dG (BP-N2-dG) that is carcinogenic. The bulky adduct block DNA synthesis by replicative or high-fidelity DNA polymerases. Some of the specialized lesion bypass polymerases (mostly belonging to Y-family) can replicate through this

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3

Kasiviswanathan, Rajesh, Irina G. Minko, R. Stephen Lloyd та William C. Copeland. "Translesion Synthesis Past Acrolein-derived DNA Adducts by Human Mitochondrial DNA Polymerase γ". Journal of Biological Chemistry 288, № 20 (2013): 14247–55. http://dx.doi.org/10.1074/jbc.m113.458802.

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Acrolein, a mutagenic aldehyde, is produced endogenously by lipid peroxidation and exogenously by combustion of organic materials, including tobacco products. Acrolein reacts with DNA bases forming exocyclic DNA adducts, such as γ-hydroxy-1,N2-propano-2′-deoxyguanosine (γ-HOPdG) and γ-hydroxy-1,N6-propano-2′-deoxyadenosine (γ-HOPdA). The bulky γ-HOPdG adduct blocks DNA synthesis by replicative polymerases but can be bypassed by translesion synthesis polymerases in the nucleus. Although acrolein-induced adducts are likely to be formed and persist in mitochondrial DNA, animal cell mitochondria l

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4

Hang, Bo. "Formation and Repair of Tobacco Carcinogen-Derived Bulky DNA Adducts." Journal of Nucleic Acids 2010 (2010): 1–29. http://dx.doi.org/10.4061/2010/709521.

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DNA adducts play a central role in chemical carcinogenesis. The analysis of formation and repair of smoking-related DNA adducts remains particularly challenging as both smokers and nonsmokers exposed to smoke are repetitively under attack from complex mixtures of carcinogens such as polycyclic aromatic hydrocarbons andN-nitrosamines. The bulky DNA adducts, which usually have complex structure, are particularly important because of their biological relevance. Several known cellular DNA repair pathways have been known to operate in human cells on specific types of bulky DNA adducts, for example,

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5

Wei, D., V. M. Maher, and J. J. McCormick. "Site-specific excision repair of 1-nitrosopyrene-induced DNA adducts at the nucleotide level in the HPRT gene of human fibroblasts: effect of adduct conformation on the pattern of site-specific repair." Molecular and Cellular Biology 16, no. 7 (1996): 3714–19. http://dx.doi.org/10.1128/mcb.16.7.3714.

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Studies showing that different types of DNA adducts are repaired in human cells at different rates suggest that DNA adduct conformation is the major determinant of the rate of nucleotide excision repair. However, recent studies of repair of cyclobutane pyrimidine dimers or benzo[a]pyrene diol epoxide (BPDE)-induced adducts at the nucleotide level in DNA of normal human fibroblasts indicate that the rate of repair of the same adduct at different nucleotide positions can vary up to 10-fold, suggesting an important role for local DNA conformation. To see if site-specific DNA repair is a common ph

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6

Sahasrabudhe, S. R., X. Luo, and M. Z. Humayun. "Specificity of base substitutions induced by the acridine mutagen ICR-191: mispairing by guanine N7 adducts as a mutagenic mechanism." Genetics 129, no. 4 (1991): 981–89. http://dx.doi.org/10.1093/genetics/129.4.981.

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Abstract As the most nucleophilic site in DNA, the guanine N7 atom is a major site of adduction by a large number of alkylating mutagens and carcinogens. Aflatoxin B1, a powerful mutagen, is believed to act through its reaction with this DNA site. On the basis of the specificity of base substitutions induced by various adduct forms of aflatoxin, we have proposed that bulky guanine N7 adducts elicit base substitutions by two mechanisms. The first mechanism is similar to that observed for a number of bulky noninstructive lesions, whereas the second mechanism invokes mispairing between N7-adducte

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7

Dunn, Bruce P. "Detection of Aromatic DNA Adducts in Human Cells and Fish Liver." Journal of the American College of Toxicology 8, no. 5 (1989): 905–12. http://dx.doi.org/10.3109/10915818909018051.

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Both nuclease PI treatment and reverse-phase high-performance liquid chromatography (HPLC) were used to enrich hydrophobic/bulky DNA adducts in DNA digests. 32P-postlabeling procedures and thin layer chromatography were then used to detect and quantitate aromatic/bulky DNA adducts. For both human and fish DNA from individuals exposed to environmental carcinogens, the nuclease PI and HPLC enrichment procedures generally gave similar results. The bottom sediments of the Buffalo and Detroit rivers are contaminated with polycyclic aromatic hydrocarbon carcinogens, and brown bullheads in these rive

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8

Hambley, Trevor W., Susan J. Berners-Price, Murray S. Davies, et al. "Steric Determinants of Pt/DNA Interactions and Anticancer Activity." Metal-Based Drugs 5, no. 4 (1998): 197–206. http://dx.doi.org/10.1155/mbd.1998.197.

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Studies directed at establishing the structural features that control Pt/DNA interactions and the anticancer activity of Pt drugs are described. [H1,N15]-HSQC 2D NMR spectroscopic studies of the reactions of cisplatin with oligonucleotides containing ApG and GpA binding sites reveal dramatic differences in the rates of formation of monofunctional adducts at the two sites. When the reactant is cis-[Pt(NH3)2(OH2)2]2+ no such differences are observed suggesting that outer-sphere interactions between the reactant and the oligonucleotide may play a substantial role in determining the rates. Rates o

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9

Jung, Hunmin, Naveen Kumar Rayala та Seongmin Lee. "Translesion synthesis of the major nitrogen mustard-induced DNA lesion by human DNA polymerase η". Biochemical Journal 477, № 23 (2020): 4543–58. http://dx.doi.org/10.1042/bcj20200767.

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Nitrogen mustards are among the first modern anticancer chemotherapeutics that are still widely used as non-specific anticancer alkylating agents. While the mechanism of action of mustard drugs involves the generation of DNA interstrand cross-links, the predominant lesions produced by these drugs are nitrogen half-mustard-N7-dG (NHMG) adducts. The bulky major groove lesion NHMG, if left unrepaired, can be bypassed by translesion synthesis (TLS) DNA polymerases. However, studies of the TLS past NHMG have not been reported so far. Here, we present the first synthesis of an oligonucleotide contai

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10

Castaño-Vinyals, Gemma, Glenn Talaska, Nathaniel Rothman, et al. "Bulky DNA Adduct Formation and Risk of Bladder Cancer." Cancer Epidemiology Biomarkers & Prevention 16, no. 10 (2007): 2155–59. http://dx.doi.org/10.1158/1055-9965.epi-07-0184.

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11

Peterson, Lisa A. "Formation, Repair, and Genotoxic Properties of Bulky DNA Adducts Formed from Tobacco-Specific Nitrosamines." Journal of Nucleic Acids 2010 (2010): 1–11. http://dx.doi.org/10.4061/2010/284935.

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4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) andN′-nitrosonornicotine (NNN) are tobacco-specific nitrosamines present in tobacco products and smoke. Both compounds are carcinogenic in laboratory animals, generating tumors at sites comparable to those observed in smokers. These Group 1 human carcinogens are metabolized to reactive intermediates that alkylate DNA. This paper focuses on the DNA pyridyloxobutylation pathway which is common to both compounds. This DNA route generates 7-[4-(3-pyridyl)-4-oxobut-1-yl]-2′-deoxyguanosine,O2-[4-(3-pyridyl)-4-oxobut-1-yl]-2′-deoxycytosine,O2-[4-(3

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12

Federley, Richard G., and Louis J. Romano. "DNA Polymerase: Structural Homology, Conformational Dynamics, and the Effects of Carcinogenic DNA Adducts." Journal of Nucleic Acids 2010 (2010): 1–15. http://dx.doi.org/10.4061/2010/457176.

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DNA replication is vital for an organism to proliferate and lying at the heart of this process is the enzyme DNA polymerase. Most DNA polymerases have a similar three dimensional fold, akin to a human right hand, despite differences in sequence homology. This structural homology would predict a relatively unvarying mechanism for DNA synthesis yet various polymerases exhibit markedly different properties on similar substrates, indicative of each type of polymerase being prescribed to a specific role in DNA replication. Several key conformational steps, discrete states, and structural moieties h

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13

Johnson, Allison A., Jane M. Sayer, Haruhiko Yagi, et al. "Effect of DNA Modifications on DNA Processing by HIV-1 Integrase and Inhibitor Binding." Journal of Biological Chemistry 281, no. 43 (2006): 32428–38. http://dx.doi.org/10.1074/jbc.m605101200.

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Integration of the viral cDNA into host chromosomes is required for viral replication. Human immunodeficiency virus integrase catalyzes two sequential reactions, 3′-processing (3′-P) and strand transfer (ST). The first integrase inhibitors are undergoing clinical trial, but interactions of inhibitors with integrase and DNA are not well understood in the absence of a co-crystal structure. To increase our understanding of integrase interactions with DNA, we examined integrase catalysis with oligonucleotides containing DNA backbone, base, and groove modifications placed at unique positions surrou

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14

LIU, Yiyong, Zhengguan YANG, Christopher D. UTZAT, et al. "Interactions of human replication protein A with single-stranded DNA adducts." Biochemical Journal 385, no. 2 (2005): 519–26. http://dx.doi.org/10.1042/bj20041151.

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Human RPA (replication protein A), a single-stranded DNA-binding protein, is required for many cellular pathways including DNA repair, recombination and replication. However, the role of RPA in nucleotide excision repair remains elusive. In the present study, we have systematically examined the binding of RPA to a battery of well-defined ssDNA (single-stranded DNA) substrates using fluorescence spectroscopy. These substrates contain adducts of (6-4) photoproducts, N-acetyl-2-aminofluorene-, 1-aminopyrene-, BPDE (benzo[a]pyrene diol epoxide)- and fluorescein that are different in many aspects s

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15

Millen, Andrea L., Purshotam Sharma, and Stacey D. Wetmore. "C8-linked bulky guanosine DNA adducts: experimental and computational insights into adduct conformational preferences and resulting mutagenicity." Future Medicinal Chemistry 4, no. 15 (2012): 1981–2007. http://dx.doi.org/10.4155/fmc.12.138.

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16

Said, Boctor, Matthew K. Ross, Tamer Salib, and Ronald C. Shank. "Modulation of DNA adduct formation by successive exposures of DNA to small and bulky chemical carcinogens." Carcinogenesis 16, no. 12 (1995): 3057–62. http://dx.doi.org/10.1093/carcin/16.12.3057.

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17

de Kok, T. M. C. M., H. J. J. Moonen, J. van Delft, and F. J. van Schooten. "Methodologies for bulky DNA adduct analysis and biomonitoring of environmental and occupational exposures." Journal of Chromatography B 778, no. 1-2 (2002): 345–55. http://dx.doi.org/10.1016/s0378-4347(01)00543-6.

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18

Yi, ChengQi, and Chuan He. "AlkB recognition of a bulky DNA base adduct stabilized by chemical cross-linking." Science China Chemistry 53, no. 1 (2010): 86–90. http://dx.doi.org/10.1007/s11426-010-0008-0.

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19

Georgieva, Daniela, Qian Liu, Kai Wang, and Dieter Egli. "Detection of base analogs incorporated during DNA replication by nanopore sequencing." Nucleic Acids Research 48, no. 15 (2020): e88-e88. http://dx.doi.org/10.1093/nar/gkaa517.

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Abstract DNA synthesis is a fundamental requirement for cell proliferation and DNA repair, but no single method can identify the location, direction and speed of replication forks with high resolution. Mammalian cells have the ability to incorporate thymidine analogs along with the natural A, T, G and C bases during DNA synthesis, which allows for labeling of replicating or repaired DNA. Here, we demonstrate the use of the Oxford Nanopore Technologies MinION to detect 11 different thymidine analogs including CldU, BrdU, IdU as well as EdU alone or coupled to Biotin and other bulky adducts in s

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20

Vyas, Rajan, Georgia Efthimiopoulos, E. John Tokarsky, Chanchal K. Malik, Ashis K. Basu, and Zucai Suo. "Mechanistic Basis for the Bypass of a Bulky DNA Adduct Catalyzed by a Y-Family DNA Polymerase." Journal of the American Chemical Society 137, no. 37 (2015): 12131–42. http://dx.doi.org/10.1021/jacs.5b08027.

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21

Lindsley, Janet E., and Robert P. P. Fuchs. "Use of single-turnover kinetics to study bulky adduct bypass by T7 DNA polymerase." Biochemistry 33, no. 3 (1994): 764–72. http://dx.doi.org/10.1021/bi00169a018.

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22

Gadkari, Varun V., E. John Tokarsky, Chanchal K. Malik, Ashis K. Basu, and Zucai Suo. "Mechanistic investigation of the bypass of a bulky aromatic DNA adduct catalyzed by a Y-family DNA polymerase." DNA Repair 21 (September 2014): 65–77. http://dx.doi.org/10.1016/j.dnarep.2014.06.003.

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23

Ho, Vikki, Vanessa Brunetti, Sarah Peacock, et al. "Exposure to meat-derived carcinogens and bulky DNA adduct levels in normal-appearing colon mucosa." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 821 (September 2017): 5–12. http://dx.doi.org/10.1016/j.mrgentox.2017.06.005.

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24

Ho, Vikki, Sarah Peacock, Thomas E. Massey, et al. "Bulky DNA adduct levels in normal-appearing colon mucosa, and the prevalence of colorectal adenomas." Biomarkers 23, no. 8 (2018): 735–41. http://dx.doi.org/10.1080/1354750x.2018.1485055.

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25

Simon, Nina, Charlotte Ebert, and Sabine Schneider. "Structural Basis for Bulky-Adduct DNA-Lesion Recognition by the Nucleotide Excision Repair Protein Rad14." Chemistry - A European Journal 22, no. 31 (2016): 10782–85. http://dx.doi.org/10.1002/chem.201602438.

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26

Stiborová, Marie, Martina Rupertová, Petr Hodek, Eva Frei, and Heinz H. Schmeiser. "Monitoring of DNA Adducts in Humans and 32P-Postlabelling Methods. A Review." Collection of Czechoslovak Chemical Communications 69, no. 3 (2004): 476–98. http://dx.doi.org/10.1135/cccc20040476.

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DNA adduct formation in humans is a promising biomarker for elucidating the molecular epidemiology of cancer. For detection of DNA adducts, the most widely used methods include mass spectroscopy, fluorescence spectroscopy, immunoassays and 32P-postlabelling. Among them, the 32P-postlabelling method appears to meet best the criteria of sensitivity and amount of DNA needed, and, therefore, is one of the most appropriate methods for biomonitoring of human DNA adducts. Most classes of carcinogens have been subjected to 32P-postlabelling analysis, ranging from bulky and/or aromatic compounds to sma

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27

Choi, Jeong-Yun, та F. Peter Guengerich. "Adduct Size Limits Efficient and Error-free Bypass Across Bulky N2-Guanine DNA Lesions by Human DNA Polymerase η". Journal of Molecular Biology 352, № 1 (2005): 72–90. http://dx.doi.org/10.1016/j.jmb.2005.06.079.

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28

Vaughn, Courtney M., Christopher P. Selby, Yanyan Yang, David S. Hsu, and Aziz Sancar. "Genome-wide single-nucleotide resolution of oxaliplatin–DNA adduct repair in drug-sensitive and -resistant colorectal cancer cell lines." Journal of Biological Chemistry 295, no. 22 (2020): 7584–94. http://dx.doi.org/10.1074/jbc.ra120.013347.

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Platinum-based chemotherapies, including oxaliplatin, are a mainstay in the management of solid tumors and induce cell death by forming intrastrand dinucleotide DNA adducts. Despite their common use, they are highly toxic, and approximately half of cancer patients have tumors that are either intrinsically resistant or develop resistance. Previous studies suggest that this resistance is mediated by variations in DNA repair levels or net drug influx. Here, we aimed to better define the roles of nucleotide excision repair and DNA damage in platinum chemotherapy resistance by profiling DNA damage

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29

Lone, Samer, and Louis J. Romano. "Mechanistic Insights into Replication Across from Bulky DNA Adducts: A Mutant Polymerase I Allows anN-Acetyl-2-aminofluorene Adduct To Be Accommodated during DNA Synthesis†." Biochemistry 42, no. 13 (2003): 3826–34. http://dx.doi.org/10.1021/bi027297t.

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30

Nivard, M. J., J. Wijen, and E. W. Vogel. "Germ cell mutagenesis in Drosophila: multiple endpoint analysis." Acta Biochimica Polonica 45, no. 2 (1998): 545–59. http://dx.doi.org/10.18388/abp.1998_4247.

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Genotoxic carcinogens, able to damage DNA by alkylation reactions, represent a very diverse class of agents which are capable of producing a wide range of DNA modifications. The mechanisms leading to genetic changes as a result of exposure to alkylating agents (AAs) have been studied in male germ cells of Drosophila using a structure-activity relationship approach (SAR). The analytical tools available concern both genetic and molecular assays. The genetic tests enable to quantify excision repair and clastogenic potency of the AA after treatment of post-meiotic male germ cells and to determine

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31

Perlow-Poehnelt, Rebecca A., Ilya Likhterov, David A. Scicchitano, Nicholas E. Geacintov, and Suse Broyde. "The Spacious Active Site of a Y-Family DNA Polymerase Facilitates Promiscuous Nucleotide Incorporation Opposite a Bulky Carcinogen-DNA Adduct." Journal of Biological Chemistry 279, no. 35 (2004): 36951–61. http://dx.doi.org/10.1074/jbc.m404332200.

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32

Kirouac, Kevin N., Ashis K. Basu, and Hong Ling. "Structural Mechanism of Replication Stalling on a Bulky Amino-Polycyclic Aromatic Hydrocarbon DNA Adduct by a Y Family DNA Polymerase." Journal of Molecular Biology 425, no. 22 (2013): 4167–76. http://dx.doi.org/10.1016/j.jmb.2013.07.020.

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33

Jensen, L., and S. Linn. "A reduced rate of bulky DNA adduct removal is coincident with differentiation of human neuroblastoma cells induced by nerve growth factor." Molecular and Cellular Biology 8, no. 9 (1988): 3964–68. http://dx.doi.org/10.1128/mcb.8.9.3964.

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Human SY5Y neuroblastoma cells which were differentiated in culture by treatment with 7S murine nerve growth factor for 5 weeks and selection with aphidicolin (L. Jensen, Dev. Biol. 120:56-64, 1987) demonstrated a considerably slower rate of removal of DNA adducts of benzo[a]pyrene, benzo[a]pyrenediolepoxide, and N7-methylguanine than did undifferentiated mitotic cells. A dramatic decline in unscheduled DNA synthesis induced by UV radiation was similarly observed. DNA polymerase beta and uracil DNA glycosylase were unchanged after differentiation, DNA polymerase alpha and DNA methylase decreas

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34

Jensen, L., and S. Linn. "A reduced rate of bulky DNA adduct removal is coincident with differentiation of human neuroblastoma cells induced by nerve growth factor." Molecular and Cellular Biology 8, no. 9 (1988): 3964–68. http://dx.doi.org/10.1128/mcb.8.9.3964-3968.1988.

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Human SY5Y neuroblastoma cells which were differentiated in culture by treatment with 7S murine nerve growth factor for 5 weeks and selection with aphidicolin (L. Jensen, Dev. Biol. 120:56-64, 1987) demonstrated a considerably slower rate of removal of DNA adducts of benzo[a]pyrene, benzo[a]pyrenediolepoxide, and N7-methylguanine than did undifferentiated mitotic cells. A dramatic decline in unscheduled DNA synthesis induced by UV radiation was similarly observed. DNA polymerase beta and uracil DNA glycosylase were unchanged after differentiation, DNA polymerase alpha and DNA methylase decreas

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35

Sawai, Tomoko, Masanobu Kawanishi, Takeji Takamura-Enya, and Takashi Yagi. "Establishment of a Method for Analyzing Translesion DNA Synthesis across a Single Bulky Adduct in Human Cells." Genes and Environment 31, no. 1 (2009): 24–30. http://dx.doi.org/10.3123/jemsge.31.24.

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36

Ho, Vikki, Sarah Peacock, Thomas E. Massey, et al. "Gene-diet interactions in exposure to heterocyclic aromatic amines and bulky DNA adduct levels in blood leukocytes." Environmental and Molecular Mutagenesis 56, no. 7 (2015): 609–20. http://dx.doi.org/10.1002/em.21950.

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37

Andre, Véronique, Jérémie Le Goff, Didier Pottier, et al. "Evaluation of bulky DNA adduct levels after pesticide use: Comparison between open-field farmers and fruit growers." Toxicological & Environmental Chemistry 89, no. 1 (2007): 125–39. http://dx.doi.org/10.1080/02772240600952026.

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38

Chang, Jian, William P. Watson, Erika Randerath, and Kurt Randerath. "Bulky DNA-adduct formation induced by Ni(II) in vitro and in vivo as assayed by 32P-postlabeling." Mutation Research/Environmental Mutagenesis and Related Subjects 291, no. 2 (1993): 147–59. http://dx.doi.org/10.1016/0165-1161(93)90154-r.

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39

Jha, Vikash, and Hong Ling. "Structural basis of accurate replication beyond a bulky major benzo[a]pyrene adduct by human DNA polymerase kappa." DNA Repair 49 (January 2017): 43–50. http://dx.doi.org/10.1016/j.dnarep.2016.11.001.

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40

Hu, Jinchuan, Jason D. Lieb, Aziz Sancar, and Sheera Adar. "Cisplatin DNA damage and repair maps of the human genome at single-nucleotide resolution." Proceedings of the National Academy of Sciences 113, no. 41 (2016): 11507–12. http://dx.doi.org/10.1073/pnas.1614430113.

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Cisplatin is a major anticancer drug that kills cancer cells by damaging their DNA. Cancer cells cope with the drug by removal of the damages with nucleotide excision repair. We have developed methods to measure cisplatin adduct formation and its repair at single-nucleotide resolution. “Damage-seq” relies on the replication-blocking properties of the bulky base lesions to precisely map their location. “XR-seq” independently maps the removal of these damages by capturing and sequencing the excised oligomer released during repair. The damage and repair maps we generated reveal that damage distri

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41

Frampton, Christopher S., James H. Gall, and David D. MacNicol. "Novel Ansa-Chain Conformation of a Semi-Synthetic Rifamycin Prepared Employing the Alder-Ene Reaction: Crystal Structure and Absolute Stereochemistry." Chemistry 3, no. 3 (2021): 734–43. http://dx.doi.org/10.3390/chemistry3030052.

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Rifamycins are an extremely important class of antibacterial agents whose action results from the inhibition of DNA-dependent RNA synthesis. A special arrangement of unsubstituted hydroxy groups at C21 and C23, with oxygen atoms at C1 and C8 is essential for activity. Moreover, it is known that the antibacterial action of rifamycin is lost if either of the two former hydroxy groups undergo substitution and are no longer free to act in enzyme inhibition. In the present work, we describe the successful use of an Alder-Ene reaction between Rifamycin O, 1 and diethyl azodicarboxylate, yielding 2,

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42

Molina, Edith, Rebeca Pérez-Morales, Julieta Rubio, et al. "The GSTM1null (deletion) and MGMT84 rs12917 (Phe/Phe) haplotype are associated with bulky DNA adduct levels in human leukocytes." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 758, no. 1-2 (2013): 62–68. http://dx.doi.org/10.1016/j.mrgentox.2013.09.007.

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43

Palli, D. "The effects of diet on DNA bulky adduct levels are strongly modified by GSTM1 genotype: a study on 634 subjects." Carcinogenesis 25, no. 4 (2003): 577–84. http://dx.doi.org/10.1093/carcin/bgh033.

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44

Dimopoulos, Meletios A., Christine Liakos, Hara G. Episkopou, et al. "A Polymerase Chain Reaction-Based Method to Detect Gene-Specific Adducts Induced by Anticancer Drugs. Clinical Application in Multiple Myeloma." Blood 114, no. 22 (2009): 1879. http://dx.doi.org/10.1182/blood.v114.22.1879.1879.

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Abstract Abstract 1879 Poster Board I-903 DNA repair plays an important role in the protection of cells and tissues after exposure to genotoxic agents including chemotherapeutics. We have previously shown that, in peripheral blood mononuclear cells (PBMC) of multiple myeloma (MM) patients treated with melphalan, accumulation of DNA adducts in the p53 gene correlates with better therapeutic response, and that repair in different genes correlated with the gene transcriptional activity and the degree of local chromatin condensation (Dimopoulos et al, J Clin Oncol 2005;23:4381–9; Souliotis et al,

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45

Friedrich, Annabelle, Ann-Sophie Assmann, Lena Schumacher, et al. "In Vitro Assessment of the Genotoxic Hazard of Novel Hydroxamic Acid- and Benzamide-Type Histone Deacetylase Inhibitors (HDACi)." International Journal of Molecular Sciences 21, no. 13 (2020): 4747. http://dx.doi.org/10.3390/ijms21134747.

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Histone deacetylase inhibitors (HDACi) are already approved for the therapy of leukemias. Since they are also emerging candidate compounds for the treatment of non-malignant diseases, HDACi with a wide therapeutic window and low hazard potential are desirable. Here, we investigated a panel of 12 novel hydroxamic acid- and benzamide-type HDACi employing non-malignant V79 hamster cells as toxicology guideline-conform in vitro model. HDACi causing a ≥10-fold preferential cytotoxicity in malignant neuroblastoma over non-malignant V79 cells were selected for further genotoxic hazard analysis, inclu

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Ozawa, S. "Analyses of bronchial bulky DNA adduct levels and CYP2C9, GSTP1 and NQO1 genotypes in a Hungarian study population with pulmonary diseases." Carcinogenesis 20, no. 6 (1999): 991–95. http://dx.doi.org/10.1093/carcin/20.6.991.

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Zaliznyak, Tanya, Radha Bonala, Francis Johnson, and Carlos de los Santos. "Structure and Stability of Duplex DNA Containing the 3-(Deoxyguanosin-N2-yl)-2-acetylaminofluorene (dG(N2)-AAF) Lesion: A Bulky Adduct that Persists in Cellular DNA." Chemical Research in Toxicology 19, no. 6 (2006): 745–52. http://dx.doi.org/10.1021/tx060002i.

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Lambert, B., B. K. Jones, B. P. Roques, J. B. Le Pecq, and A. T. Yeung. "The noncovalent complex between DNA and the bifunctional intercalator ditercalinium is a substrate for the UvrABC endonuclease of Escherichia coli." Proceedings of the National Academy of Sciences 86, no. 17 (1989): 6557–61. http://dx.doi.org/10.1073/pnas.86.17.6557.

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We have demonstrated that the noncovalent complex formed between DNA and an antitumor bifunctional intercalator, ditercalinium, is recognized in vitro as bulky covalent DNA lesions by the purified Escherichia coli UvrABC endonuclease. It was established that no covalent drug-DNA adduct was formed during the incubation of the drug with DNA or during subsequent incubation with the UvrAB proteins. The nucleoprotein-ditercalinium complexes appear different from those generated by repair of pyrimidine dimers. The UvrA protein is able to form a stable complex with ditercalinium-intercalated DNA in t

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Bi, Xiaohui, Laura R. Barkley, Damien M. Slater та ін. "Rad18 Regulates DNA Polymerase κ and Is Required for Recovery from S-Phase Checkpoint-Mediated Arrest". Molecular and Cellular Biology 26, № 9 (2006): 3527–40. http://dx.doi.org/10.1128/mcb.26.9.3527-3540.2006.

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ABSTRACT We have investigated mechanisms that recruit the translesion synthesis (TLS) DNA polymerase Polκ to stalled replication forks. The DNA polymerase processivity factor PCNA is monoubiquitinated and interacts with Polκ in cells treated with the bulky adduct-forming genotoxin benzo[a]pyrene dihydrodiol epoxide (BPDE). A monoubiquitination-defective mutant form of PCNA fails to interact with Polκ. Small interfering RNA-mediated downregulation of the E3 ligase Rad18 inhibits BPDE-induced PCNA ubiquitination and association between PCNA and Polκ. Conversely, overexpressed Rad18 induces PCNA

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Vijayaraj Reddy, M. "C18 thin-layer chromatographic enhancement of the 32P-postlabeling assay for aromatic or bulky carcinogen—DNA adducts: evaluation of adduct recoveries in comparison with nuclease P1 and butanol methods." Journal of Chromatography B: Biomedical Sciences and Applications 614, no. 2 (1993): 245–51. http://dx.doi.org/10.1016/0378-4347(93)80315-u.

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