Source:http://linkedlifedata.com/resource/pubmed/id/17043764
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2006-12-7
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pubmed:abstractText |
Interleukin-1 (IL-1) includes a family of closely related genes; the two major agonistic proteins, IL-1alpha and IL-1beta, are pleiotropic and affect mainly inflammation, immunity and hemopoiesis. The IL-1Ra antagonist is a physiological inhibitor of pre-formed IL-1. Recombinant IL-1alpha and IL-1beta bind to the same receptors and induce the same biological functions. As such, the IL-1 molecules have been considered identical in normal homeostasis and in disease. However, the IL-1 molecules differ in their compartmentalization within the producing cell or the microenvironment. Thus, IL-1beta is solely active in its secreted form, whereas IL-1alpha is mainly active in cell-associated forms (intracellular precursor and membrane-bound IL-1alpha) and only rarely as a secreted cytokine, as it is secreted only in a limited manner. IL-1 is abundant at tumor sites, where it may affect the process of carcinogenesis, tumor growth and invasiveness and also the patterns of tumor-host interactions. Here, we review the effects of microenvironment- and tumor cell-derived IL-1 on malignant processes in experimental tumor models and in cancer patients. We propose that membrane-associated IL-1alpha expressed on malignant cells stimulates anti-tumor immunity, while secretable IL-1beta, derived from the microenvironment or the malignant cells, activates inflammation that promotes invasiveness and also induces tumor-mediated suppression. Inhibition of the function of IL-1 by the IL-1Ra, reduces tumor invasiveness and alleviates tumor-mediated suppression, pointing to its feasibility in cancer therapy. Differential manipulation of IL-1alpha and IL-1beta in malignant cells or in the tumor's microenvironment can open new avenues for using IL-1 in cancer therapy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0167-7659
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
387-408
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pubmed:meshHeading |
pubmed-meshheading:17043764-Autocrine Communication,
pubmed-meshheading:17043764-Cell Transformation, Neoplastic,
pubmed-meshheading:17043764-Humans,
pubmed-meshheading:17043764-Interleukin-1alpha,
pubmed-meshheading:17043764-Interleukin-1beta,
pubmed-meshheading:17043764-Neoplasm Invasiveness,
pubmed-meshheading:17043764-Neoplasm Metastasis,
pubmed-meshheading:17043764-Neoplasms,
pubmed-meshheading:17043764-Paracrine Communication
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pubmed:year |
2006
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pubmed:articleTitle |
The involvement of IL-1 in tumorigenesis, tumor invasiveness, metastasis and tumor-host interactions.
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pubmed:affiliation |
Department of Microbiology and Immunology, Faculty of Health Sciences and The Cancer Research Center, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel. rapte@bgumail.bgu.ac.il
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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