Linked Life Data

11034092

Source:http://linkedlifedata.com/resource/pubmed/id/11034092

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
2000-10-16
pubmed:abstractText
MCG 101 tumors were implanted sc. on wild-type C57 Bl and gene knockout mice to evaluate the role of host-produced cytokines [interleukin (IL)-6, IL-12, IFNgamma, tumor necrosis factor (TNF) receptor 1, and TNF receptor 2] to explain local tumor growth, anorexia, and carcass weight loss in a well-defined model with experimental cachexia. Indomethacin was provided in the drinking water to explore interactions between host and tumor-derived prostaglandins and proinflammatory cytokines for tumor growth. Wild-type tumor-bearing mice developed cachexia because of rapid tumor growth, which were both attenuated in IL-6 gene knockouts. Similar findings were observed after provision of anti-IL-6 to wild-type tumor-bearing mice. Alterations in food intake were not directly related to systemic IL-6 but rather secondarily to IL-6-dependent tumor growth. The absence of host-derived IL-12, IFN-gamma, or the TNF receptor 1 or receptor 2 gene did not attenuate tumor growth or improve subsequent cachexia. Thus, carcass weight loss was not improved by the omission of host cytokine (TNF-alpha, IL-12, or IFN-gamma) except for IL-6. Systemic indomethacin provision decreased plasma prostaglandin E2 in five of six groups of gene knockout tumor-bearing mice, which was associated with improved carcass weight in these groups. Indomethacin seemed to improve food intake to a similar extent in both wild-type and gene knockouts, which agree with the speculation that eicosanoids are more important to explain anorexia than host cytokines. Our results demonstrate that host- and tumor-derived cytokines and prostaglandins interact with tumor growth and promote cachexia in a more complex fashion than usually presented based on previous information in studies on either anti-cytokine experiments in vivo or on gene knockouts with respect to a "single cytokine model." Overall, host cytokines were quantitatively less important than tumor-derived cytokines to explain net tumor growth, which indirectly explains subsequent cachexia and anorexia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5488-93
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11034092-Animals, pubmed-meshheading:11034092-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:11034092-Antibodies, pubmed-meshheading:11034092-Body Weight, pubmed-meshheading:11034092-Cachexia, pubmed-meshheading:11034092-Cell Division, pubmed-meshheading:11034092-Cytokines, pubmed-meshheading:11034092-Dinoprostone, pubmed-meshheading:11034092-Eating, pubmed-meshheading:11034092-Eicosanoids, pubmed-meshheading:11034092-Indomethacin, pubmed-meshheading:11034092-Interferon-gamma, pubmed-meshheading:11034092-Interleukin-12, pubmed-meshheading:11034092-Interleukin-6, pubmed-meshheading:11034092-Mice, pubmed-meshheading:11034092-Mice, Inbred C57BL, pubmed-meshheading:11034092-Mice, Knockout, pubmed-meshheading:11034092-Neoplasm Transplantation, pubmed-meshheading:11034092-Sarcoma, Experimental, pubmed-meshheading:11034092-Tumor Necrosis Factor-alpha
pubmed:year
2000
pubmed:articleTitle
Experimental cancer cachexia: the role of host-derived cytokines interleukin (IL)-6, IL-12, interferon-gamma, and tumor necrosis factor alpha evaluated in gene knockout, tumor-bearing mice on C57 Bl background and eicosanoid-dependent cachexia.
pubmed:affiliation
Department of Surgery, Sahlgrenska University Hospital, Göteborg University, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't