The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Oxidative and nitrative DNA damage in animals and patients with inflammatory diseases in relation to inflammation-related carcinogenesis
Abstract
Infection and chronic inflammation are proposed to contribute to carcinogenesis through inflammation-related mechanisms. Infection with hepatitis C virus, Helicobacter pylori and the liver fluke, Opisthorchis viverrini (OV), are important risk factors for hepatocellular carcinoma (HCC), gastric cancer and cholangiocarcinoma, respectively. Inflammatory bowel diseases (IBDs) and oral diseases, such as oral lichen planus (OLP) and leukoplakia, are associated with colon carcinogenesis and oral squamous cell carcinoma (OSCC), respectively. We performed a double immunofluorescence labeling study and found that nitrative and oxidative DNA lesion products, 8-nitroguanine and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), were formed and inducible nitric oxide synthase (iNOS) was expressed in epithelial cells and inflammatory cells at the site of carcinogenesis in humans and animal models. Antibacterial, antiviral and antiparasitic drugs dramatically diminished the formation of these DNA lesion markers and iNOS expression. These results suggest that oxidative and nitrative DNA damage occurs at the sites of carcinogenesis, regardless of etiology. Therefore, it is considered that excessive amounts of reactive nitrogen species produced via iNOS during chronic inflammation may play a key role in carcinogenesis by causing DNA damage. On the basis of our results, we propose that 8-nitroguanine is a promising biomarker to evaluate the potential risk of inflammation-mediated carcinogenesis.
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Cites
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Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG
Shibutani, S., Takeshita, M., & Grollman, A. P. (1991) · Nature · doi:10.1038/349431a0 · Cited by 2,224
Oxidative Nucleobase Modifications Leading to Strand Scission
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“mous variety of pathological processes, including cancer (Hussain et al., 2003; Ohshima et al., 2003).”
BackgroundOxidative DNA damage and disease: induction, repair and significance
Evans, M. D., Dizdaroglu, M., & Cooke, M. S. (2004) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2003.11.001 · Cited by 1,372 · cited 3×
“sine (8-oxodG) (Wiseman and Halliwell, 1996; Burrows and Muller, 1998; Kawanishi et al., 2001; Evans et al., 2004), which is considered to be mutagenic.”
BackgroundPowrie, F., Leach, M. W., Mauze, S., Caddie, L. B., & Coffman, R. L. (1993) · International Immunology · doi:10.1093/intimm/5.11.1461 · Cited by 1,078
Cited by
The DNA-damage response in human biology and disease
Jackson, S. P., & Bartek, J. (2009) · Nature · doi:10.1038/nature08467 · Cited by 6,092
Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?
Trachootham, D., Alexandre, J., & Huang, P. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2803 · Cited by 5,452
Reactive oxygen species generating systems meeting challenges of photodynamic cancer therapy
Zhou, Z., Song, J., Nie, L., & Chen, X. (2016) · Chemical Society Reviews · doi:10.1039/c6cs00271d · Cited by 2,098
Interferons, immunity and cancer immunoediting
Dunn, G. P., Koebel, C. M., & Schreiber, R. D. (2006) · Nature Reviews Immunology · doi:10.1038/nri1961 · Cited by 1,617
Oxidative stress and cancer: Have we moved forward?
Halliwell, B. (2007) · Biochemical Journal · doi:10.1042/bj20061131 · Cited by 1,302
Metadata
- Authors
- Kawanishi, S., Hiraku, Y., Pinlaor, S., & Ma, N.
- Venue
- Biological Chemistry
- Publisher
- Walter de Gruyter GmbH
- Published
- 2006-04-01
- Volume
- 387
- Issue
- 4
- Pages
- 365-372
- ISSN
- 1431-6730 (ISSN-L)
- 1437-4315
- OpenAlex
- W2128569634
- Cited by
- 449
- References
- 6
- FWCI
- 9.04
- Type
- journal article
- Language
- en
- Open access
- closed
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