| pubmed-article:1680022 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1680022 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:1680022 | lifeskim:mentions | umls-concept:C0007582 | lld:lifeskim |
| pubmed-article:1680022 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:1680022 | lifeskim:mentions | umls-concept:C1519667 | lld:lifeskim |
| pubmed-article:1680022 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:1680022 | pubmed:dateCreated | 1991-10-21 | lld:pubmed |
| pubmed-article:1680022 | pubmed:abstractText | Human melanoma cell lines that express high constitutive levels of the metastasis-associated marker intercellular adhesion molecule 1 (ICAM-1) were found to secrete interleukin 1 (IL-1) in vitro. Experiments with neutralizing antibodies showed that this cytokine was responsible for their expression of ICAM-1 but not that of two other progression/metastasis markers, Muc-18 and Gp IIb/IIIa. The IL-1 present in melanoma-conditioned medium induced the expression of vascular cell adhesion molecule 1, endothelial-leukocyte adhesion molecule 1, and ICAM-1 on human umbilical vein endothelial cells (ECs) in culture and increased the rate at which melanoma cells and ECs adhered to each other. IL-1-producing melanoma lines adhered significantly more rapidly to ECs than did non-IL-1-producing lines, and this enhancement was reduced by prior incubation of the melanoma cells with neutralizing anti-IL-1 antibodies. Similarly, endothelial cells treated with conditioned medium from IL-1-producing melanoma lines adhered significantly more rapidly to melanoma cells than did ECs treated with medium from non-IL-1-producing melanoma lines, and this enhancement was abolished by addition of anti-IL-1 antibodies to EC cultures in conditioned medium. Blocking antibodies to endothelial vascular cell adhesion molecule 1, endothelial-leukocyte adhesion molecule 1, and ICAM-1 failed to inhibit melanoma-EC adhesion, but an antibody to tumor cell GpIIb/IIIa did block adhesion by up to 44%. The ability to secrete IL-1 could increase the metastatic potential of melanoma cells by stimulating tumor cell-EC adhesion. | lld:pubmed |
| pubmed-article:1680022 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1680022 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1680022 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1680022 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1680022 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:1680022 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:MarshallJ FJF | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:HartI RIR | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:PooleSS | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:ThorpeP EPE | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:HaskardD ODO | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:BurrowsF JFJ | lld:pubmed |
| pubmed-article:1680022 | pubmed:author | pubmed-author:SelkirkSS | lld:pubmed |
| pubmed-article:1680022 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1680022 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:1680022 | pubmed:volume | 51 | lld:pubmed |
| pubmed-article:1680022 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1680022 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1680022 | pubmed:pagination | 4768-75 | lld:pubmed |
| pubmed-article:1680022 | pubmed:dateRevised | 2005-11-17 | lld:pubmed |
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| pubmed-article:1680022 | pubmed:meshHeading | pubmed-meshheading:1680022-... | lld:pubmed |
| pubmed-article:1680022 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1680022 | pubmed:articleTitle | Influence of tumor-derived interleukin 1 on melanoma-endothelial cell interactions in vitro. | lld:pubmed |
| pubmed-article:1680022 | pubmed:affiliation | Drug Targeting, Imperial Cancer Research Fund, Lincoln's Inn Fields, London, England. | lld:pubmed |
| pubmed-article:1680022 | pubmed:publicationType | Journal Article | lld:pubmed |
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