Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
1997-7-8
|
pubmed:abstractText |
In order to study adhesion-molecule expression and its consequences for cellular recognition, the presence of adhesion molecules ICAM-1, VCAM-1, VLA-4, LFA-1, alpha, LFA-1 beta, LFA-3, beta1-integrin and beta3-integrin was studied on specimens from breast tissue by immunohistochemistry and on cells from breast cell lines propagated in vitro. Breast-cancer tissue and the breast-cancer cell lines MCF-7, SK-BR-3 and ZR-75-1 showed expression of ICAM-1 and VLA-4 significantly lower than that of benign breast cells or normal breast epithelium. Of various cytokines tested, including recombinant human (rh) interleukin-6 (IL-6), rh tumor necrosis factor alpha (TNF-alpha), interleukin 2 (IL-2), granulocyte/macrophage-colony-stimulating-factor (GM-CSF), interferon-alpha (IFN-alpha) and interferon-gamma (IFN-gamma), only TNF was able to re-induce expression of ICAM-1 on cells from MCF-7, SK-BR-3 and ZR-75-1. Further, the ability of either unstimulated or lymphokine-stimulated killer (LAK) cells to recognize and lyse native or TNF-stimulated breast-cancer cells was studied. Whereas neither unstimulated lymphocytes or LAK cells were able to lyse untreated breast-cancer cells deficient for ICAM-1 expression, pre-treatment of tumor cells with TNF led to increased tumor-cell lysis. Anti-ICAM-1 antibodies, and pre-treatment of tumor cells with anti-TNF-receptor antibodies, abrogated these findings, corroborating their specificity. We thus conclude that the defective expression of ICAM-1 in our model might constitute a mechanism by which breast-cancer cells escape immunologic recognition and lysis by appropriate effector cells.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
0020-7136
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
11
|
pubmed:volume |
71
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1086-90
|
pubmed:dateRevised |
2007-7-24
|
pubmed:meshHeading |
pubmed-meshheading:9185715-Antibodies,
pubmed-meshheading:9185715-Breast Neoplasms,
pubmed-meshheading:9185715-Humans,
pubmed-meshheading:9185715-Immunohistochemistry,
pubmed-meshheading:9185715-Intercellular Adhesion Molecule-1,
pubmed-meshheading:9185715-Killer Cells, Lymphokine-Activated,
pubmed-meshheading:9185715-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:9185715-Tumor Cells, Cultured,
pubmed-meshheading:9185715-Tumor Necrosis Factor-alpha
|
pubmed:year |
1997
|
pubmed:articleTitle |
Decreased expression of ICAM-1 and its induction by tumor necrosis factor on breast-cancer cells in vitro.
|
pubmed:affiliation |
Department of Internal Medicine I, University Hospital, Vienna, Austria.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|