Source:http://linkedlifedata.com/resource/pubmed/id/17178846
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
24
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pubmed:dateCreated |
2006-12-20
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pubmed:abstractText |
Tumor necrosis factor-alpha (TNF-alpha) is an important inflammation cytokine without known direct effect on DNA. In this study, we found that TNF-alpha can cause DNA damages through reactive oxygen species. The mutagenic effect of TNF-alpha is comparable with that of ionizing radiation. TNF-alpha treatment in cultured cells resulted in increased gene mutations, gene amplification, micronuclei formation, and chromosomal instability. Antioxidants significantly reduced TNF-alpha-induced genetic damage. TNF-alpha also induced oxidative stress and nucleotide damages in mouse tissues in vivo. Moreover, TNF-alpha treatment alone led to increased malignant transformation of mouse embryo fibroblasts, which could be partially suppressed by antioxidants. As TNF-alpha is involved in chronic inflammatory diseases, such as chronic hepatitis, ulcerative colitis, and chronic skin ulcers, and these diseases predispose the patients to cancer development, our results suggest a novel pathway through which TNF-alpha promotes cancer development through induction of gene mutations, in addition to the previously reported mechanisms, in which nuclear factor-kappaB activation was implicated.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytochalasin B,
http://linkedlifedata.com/resource/pubmed/chemical/Fluoresceins,
http://linkedlifedata.com/resource/pubmed/chemical/Mutagens,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/diacetyldichlorofluorescein
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0008-5472
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
66
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11565-70
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pubmed:meshHeading |
pubmed-meshheading:17178846-Animals,
pubmed-meshheading:17178846-Cell Line, Tumor,
pubmed-meshheading:17178846-Cell Transformation, Neoplastic,
pubmed-meshheading:17178846-Colonic Neoplasms,
pubmed-meshheading:17178846-Cytochalasin B,
pubmed-meshheading:17178846-DNA Damage,
pubmed-meshheading:17178846-Fluoresceins,
pubmed-meshheading:17178846-Gene Amplification,
pubmed-meshheading:17178846-Humans,
pubmed-meshheading:17178846-Mice,
pubmed-meshheading:17178846-Mutagens,
pubmed-meshheading:17178846-Mutation,
pubmed-meshheading:17178846-Oxidative Stress,
pubmed-meshheading:17178846-Plasmids,
pubmed-meshheading:17178846-Reactive Oxygen Species,
pubmed-meshheading:17178846-Tumor Necrosis Factor-alpha
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pubmed:year |
2006
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pubmed:articleTitle |
Tumor necrosis factor-alpha is a potent endogenous mutagen that promotes cellular transformation.
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pubmed:affiliation |
Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
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