Source:http://linkedlifedata.com/resource/pubmed/id/11225989
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2001-2-27
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pubmed:abstractText |
The recently described CC chemokine, 6C-kine, is unique in that it contains -six rather than the usual four conserved cysteines typical of this family. Furthermore, murine 6C-kine binds to one of the CXC chemokine receptors CXCR3, in addition to its other known receptor CCR7. We have shown that two other ligands of CXCR3, IP-10 and MIG, are potent inhibitors of tumor growth in severe combined immunodeficiency (SCID) mice. We postulated that murine 6C-kine may also inhibit tumor growth via inhibition of angiogenesis in this model. SCID mice (n = 6 per group) inoculated with A549 human lung cancer cells were treated with either 6C-kine (100 ng intra-tumor injection every other day) or control protein for 8 weeks. Tumors from murine 6C-kine-treated mice (288 +/- 26 mm3) were significantly smaller than tumors from control treated mice (788 +/- 156 mm3, P = 0.005). Additionally, murine 6C-kine reduced metastases compared with controls (0.5 +/- 0.3 vs 3.0 +/- 1.2 metastases per animal, P = 0.05). Tumor vascularity (as assessed by vessel density counting) was reduced in murine 6C-kine-treated mice compared with controls. Murine 6C-kine had no direct effect on proliferation of A549 cells, and there were no differences in the infiltration of leukocyte sub-populations, assessed by flow cytometry, in the treatment groups. Interestingly, human 6C-kine, unlike murine 6C-kine, does not bind CXCR3 and had no anti-tumor effect in the same model. These data suggest that murine 6Ckine has anti-tumor effects independent of its leukocyte-recruiting activity. Furthermore, while not confirmatory, these data lend further support to the fact that CXCR3 may be the receptor for angiostatic CXC chemokines.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiogenesis Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/CCL21 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CXCR3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ccl21c protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL21,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcr3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0340-7004
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
587-92
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11225989-Angiogenesis Inhibitors,
pubmed-meshheading:11225989-Animals,
pubmed-meshheading:11225989-Carcinoma, Non-Small-Cell Lung,
pubmed-meshheading:11225989-Cell Division,
pubmed-meshheading:11225989-Chemokine CCL21,
pubmed-meshheading:11225989-Chemokines, CC,
pubmed-meshheading:11225989-Chimera,
pubmed-meshheading:11225989-Female,
pubmed-meshheading:11225989-Humans,
pubmed-meshheading:11225989-Leukocytes,
pubmed-meshheading:11225989-Lung Neoplasms,
pubmed-meshheading:11225989-Mice,
pubmed-meshheading:11225989-Mice, SCID,
pubmed-meshheading:11225989-Neoplasm Metastasis,
pubmed-meshheading:11225989-Neoplasms, Experimental,
pubmed-meshheading:11225989-Neovascularization, Pathologic,
pubmed-meshheading:11225989-Receptors, CXCR3,
pubmed-meshheading:11225989-Receptors, Chemokine,
pubmed-meshheading:11225989-Tumor Cells, Cultured
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pubmed:year |
2001
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pubmed:articleTitle |
The murine CC chemokine, 6C-kine, inhibits tumor growth and angiogenesis in a human lung cancer SCID mouse model.
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pubmed:affiliation |
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0642, USA. darenber@umich.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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