Source:http://linkedlifedata.com/resource/pubmed/id/11891530
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2002-3-13
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pubmed:abstractText |
p57 (Kip2) belongs to the Cip/Kip family and is one of the universal negative regulators of the cell cycle. In this study, we investigated the p57 expression of various types of thyroid neoplasm. p57 overexpression was observed in only 4.2% of normal thyroid tissues. In follicular adenoma and minimally invasive follicular carcinoma, p57 was overexpressed in 100% and 91.7% of the cases, respectively. However, its incidence was significantly lower (p<0.0001) in widely invasive follicular carcinoma, of which only 36.4% overexpressed p57. This phenomenon was seen in 63.1% of papillary carcinoma and 13.3% of anaplastic (undifferentiated) carcinoma. Furthermore, poorly differentiated and undifferentiated carcinoma more frequently lacked p57 expression (p<0.0001). These results suggest that the down-regulation of p57 may play a role in the dedifferentiation of thyroid carcinoma and in follicular carcinoma mutating to be more invasive.
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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 |
Apr
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pubmed:issn |
1107-3756
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
373-6
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:11891530-Cell Differentiation,
pubmed-meshheading:11891530-Cyclin-Dependent Kinase Inhibitor p57,
pubmed-meshheading:11891530-Down-Regulation,
pubmed-meshheading:11891530-Humans,
pubmed-meshheading:11891530-Immunohistochemistry,
pubmed-meshheading:11891530-Nuclear Proteins,
pubmed-meshheading:11891530-Thyroid Gland,
pubmed-meshheading:11891530-Thyroid Neoplasms
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pubmed:year |
2002
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pubmed:articleTitle |
Expression of p57/Kip2 protein in normal and neoplastic thyroid tissues.
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pubmed:affiliation |
Kuma Hospital, 8-2-35 Shimoyamate-Dori, Chuo-ku, Kobe City 650-0011, Japan. ito01@kuma-h.or.jp
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pubmed:publicationType |
Journal Article
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