Source:http://linkedlifedata.com/resource/pubmed/id/16287490
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
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| pubmed:dateCreated |
2005-11-18
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| pubmed:abstractText |
The KIT, epidermal growth factor receptor (EGFR) and HER-2 oncoproteins have tyrosine kinase activity and are molecular targets in human cancer therapy. To clarify the significance of KIT, EGFR, and HER-2 in undifferentiated thyroid carcinoma (UTC), the expression of these receptors and tyrosine phosphorylation was examined immunohistochemically in resected cases of UTC and papillary thyroid carcinoma (PTC). KIT, EGFR, and HER-2 were also examined at the protein and mRNA levels in five UTC cell lines. KIT expression (1+), EGFR overexpression (2+/3+), HER-2 expression (1+), and tyrosine phosphorylation were detected immunohistochemically in 40%, 70%, 10%, and 50% of the 10 UTC. In 20 PTC, KIT, EGFR, and HER-2 were not detected, but tyrosine phosphorylation was detected in 25% of cases. In the five UTC cell lines, KIT expression (1+), EGFR overexpression (3+), HER-2 expression (1+), and tyrosine phosphorylation were detected immunocytochemically in 60%, 100%, 20%, and 40%, respectively. Western blot analysis did not detect KIT expression, but did detect EGFR and HER-2 expression in all five cell lines. Real-time polymerase chain reaction detected KIT mRNA in two of the cell lines (40%), EGFR in five (100%), and HER-2 in three (60%). The present findings suggest that EGFR overexpression was involved in the proliferation and development of UTC and was frequently accompanied by tyrosine phosphorylation. Expression of KIT and HER-2 appeared to be weak but significant, suggesting a possible role in the development of UTC. Molecular therapies targeting KIT, EGFR, HER-2, and/or tyrosine phosphorylation might be indicated for UTC.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Topoisomerases, Type II,
http://linkedlifedata.com/resource/pubmed/chemical/DNA topoisomerase II alpha,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ki-67 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-kit,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
1320-5463
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
55
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
757-65
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:16287490-Antigens, Neoplasm,
pubmed-meshheading:16287490-Carcinoma, Papillary,
pubmed-meshheading:16287490-Cell Differentiation,
pubmed-meshheading:16287490-Cell Line, Tumor,
pubmed-meshheading:16287490-Cell Proliferation,
pubmed-meshheading:16287490-DNA Topoisomerases, Type II,
pubmed-meshheading:16287490-DNA-Binding Proteins,
pubmed-meshheading:16287490-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16287490-Humans,
pubmed-meshheading:16287490-Ki-67 Antigen,
pubmed-meshheading:16287490-Phosphorylation,
pubmed-meshheading:16287490-Protein-Tyrosine Kinases,
pubmed-meshheading:16287490-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:16287490-RNA, Messenger,
pubmed-meshheading:16287490-Receptor, Epidermal Growth Factor,
pubmed-meshheading:16287490-Receptor, erbB-2,
pubmed-meshheading:16287490-Thyroid Neoplasms,
pubmed-meshheading:16287490-Tyrosine
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| pubmed:year |
2005
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| pubmed:articleTitle |
Expression of KIT, EGFR, HER-2 and tyrosine phosphorylation in undifferentiated thyroid carcinoma: implication for a new therapeutic approach.
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| pubmed:affiliation |
Department of Pathology II, National Defense Medical College and Hospital, Tokorozawa, Japan.
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| pubmed:publicationType |
Journal Article
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