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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1998-7-17
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pubmed:abstractText |
The syndrome of cachexia associated with malignant diseases can be in part attributed to the effects of tumour necrosis factor alpha (TNFalpha) which itself is produced by a variety of tumour cells. We have recently reported that the human hepatoma cell line HepG2 expresses the TNFalpha gene and releases biologically active TNFalpha protein after stimulation with interleukin-1beta (IL-1beta). Granulocyte-colony stimulating factor (G-CSF) is a glycoprotein necessary for the proliferation and differentiation of neutrophil progenitor cells in the bone marrow. In addition G-CSF has been reported to exert anti-inflammatory effects. In our study we tested the effect of recombinant human G-CSF (rhG-CSF) on TNFalpha production in HepG2 cells. It could be shown that rhG-CSF (250 U/ml) significantly reduced IL-1beta-induced (300 pg/ml) TNFalpha gene expression after 1-h and 3-h incubation periods (TNFalpha mRNA concentrations were: 8.8+/-2.1 amol/ microg total RNA after a 1-h incubation with IL-1beta versus 3.8+/-1.3 amol/ microg total RNA after a 1-h incubation with IL-1beta + rhG-CSF and 13.8+/-2.2 amol/ microg total RNA after a 3-h incubation with IL-1beta versus 8.8+/-2. 1 amol/ microg total RNA after a 3-h incubation with IL-1beta + rhG-CSF). From these data we conclude that rhG-CSF is a potent inhibitor of cytokine-induced TNFalpha production by tumour cells. Therefore, treatment of patients with malignant diseases with rhG-CSF might represent a useful tool to improve the tumour-associated cachexia.
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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/Granulocyte Colony-Stimulating...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0031-6768
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
436
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
233-7
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9594023-Carcinoma, Hepatocellular,
pubmed-meshheading:9594023-Gene Expression,
pubmed-meshheading:9594023-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:9594023-Humans,
pubmed-meshheading:9594023-Interleukin-1,
pubmed-meshheading:9594023-Kinetics,
pubmed-meshheading:9594023-Liver Neoplasms,
pubmed-meshheading:9594023-NF-kappa B,
pubmed-meshheading:9594023-RNA, Messenger,
pubmed-meshheading:9594023-Recombinant Proteins,
pubmed-meshheading:9594023-Tumor Cells, Cultured,
pubmed-meshheading:9594023-Tumor Necrosis Factor-alpha
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pubmed:year |
1998
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pubmed:articleTitle |
Granulocyte-colony stimulating factor inhibits TNFalpha production in a human hepatoma cell line.
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pubmed:affiliation |
Department of Physiology I, University of Bonn, Nussallee 11, D-53115 Bonn, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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