Source:http://linkedlifedata.com/resource/pubmed/id/11920587
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2002-3-28
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pubmed:abstractText |
The extracellular matrix protein tenascin-C is expressed in processes like embryogenesis and wound healing and in neoplasia. Tenascin-C expression in gliomas has been described previously; however, the relation to clinical data remains inconsistent. Generally, analysis of tenascin-C function is difficult due to different alternatively spliced isoforms. Our studies focus on changes in tenascin-C expression in human gliomas, correlating these changes with tumor progression and elucidating the functional role of the glioma cell-specific tenascin-C isoform pool. Eighty-six glioma tissues of different World Health Organization (WHO) grades were analyzed immunohistochemically for tenascin-C expression. The influence of the specific tenascin-C isoforms produced by glioblastoma cells on proliferation and migration was examined in vitro using blocking antibodies recognizing all isoforms. In general, tenascin-C expression increased with tumor malignancy. Perivascular staining of tenascin-C around tumor-supplying blood vessels was observed in all glioblastoma tissues, whereas in WHO II and III gliomas, perivascular tenascin-C staining appeared less frequently. The appearance of perivascular tenascin-C correlated significantly with a shorter disease-free time. Analysis of proliferation and migration in the presence of blocking antibodies revealed an inhibition of proliferation by around 30% in all 3 glioblastoma cell cultures, as well as a decrease in migration of 30.6-46.7%. Thus we conclude that the endogenous pool of tenascin-C isoforms in gliomas supports both tumor cell proliferation and tumor cell migration. In addition, our data on the perivascular staining of tenascin-C in WHO II and III gliomas and its correlation with a shorter disease-free time suggest that tenascin-C may be a new and potent prognostic marker for an earlier tumor recurrence.
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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 |
Mar
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pubmed:issn |
0020-7136
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2002 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:day |
20
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pubmed:volume |
98
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
362-9
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pubmed:dateRevised |
2007-7-24
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pubmed:meshHeading |
pubmed-meshheading:11920587-Antibodies, Monoclonal,
pubmed-meshheading:11920587-Brain Neoplasms,
pubmed-meshheading:11920587-Cell Division,
pubmed-meshheading:11920587-Cell Movement,
pubmed-meshheading:11920587-Cells, Cultured,
pubmed-meshheading:11920587-Disease Progression,
pubmed-meshheading:11920587-Glioblastoma,
pubmed-meshheading:11920587-Glioma,
pubmed-meshheading:11920587-Humans,
pubmed-meshheading:11920587-Immunoenzyme Techniques,
pubmed-meshheading:11920587-Neoplasm Recurrence, Local,
pubmed-meshheading:11920587-Neoplasm Staging,
pubmed-meshheading:11920587-Tenascin
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pubmed:year |
2002
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pubmed:articleTitle |
Clinical impact and functional aspects of tenascin-C expression during glioma progression.
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pubmed:affiliation |
Molecular Biology Laboratory, Neurosurgery Hospital, University of Heidelberg, Germany. Christel_Herold-Mende@med.uni-heidelberg.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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