Linked Life Data

9461119

Source:http://linkedlifedata.com/resource/pubmed/id/9461119

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-3-9
pubmed:abstractText
p57KIP2 (KIP2) is a cyclin-dependent kinase inhibitor that arrests cells in G1 and an imprinted gene mapped on chromosome 11p15.5. To investigate the role of KIP2 in Wilms' tumor (WT), DNA and RNA were extracted from archival tissue sections of WT. KIP2 expression was investigated by reverse transcription-polymerase chain reaction and in situ mRNA hybridization. Thirteen of 39 WT were informative for length polymorphism of KIP2 and subjected to reverse transcription-polymerase chain reaction. KIP2 was expressed predominantly from one allele, although a low level of expression was also detected from the other. Three WT with loss of heterozygosity at the KIP2 locus demonstrated that the remaining KIP2 allele was still active, which was also confirmed by in situ hybridization. Furthermore, among 13 KIP2-informative WT, 2 were heterozygous for insulin-like growth factor II (IGF2). Allele-specific analysis demonstrated that one showed monoallelic IGF2 expression, whereas the other showed biallelic expression. In situ hybridization of fetal kidney showed that KIP2 transcripts were detected in a variety of cell types, among which differentiated epithelial structures showed higher expression than undifferentiated mesenchyme, whereas IGF2 was expressed predominantly in undifferentiated mesenchyme and renal vesicles of an early phase. WT demonstrated KIP2 and IGF2 hybridization patterns similar to fetal kidney in that KIP2 transcripts were detected in epithelial structures and blastema, whereas IGF2 transcripts were seen in blastema and immature epithelial structures. Hybridization results indicated that KIP2 expression in WT did not appear to be significantly reduced compared with that in fetal kidney and that WT demonstrated a significant amount of KIP2 transcripts regardless of retention or loss of heterozygosity at the KIP2 locus. These data suggest that although KIP2 may play a role in differentiation of the fetal kidney, it is not likely as a tumor suppressor gene, which is implicated as the cause of the development of a majority of WT.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
19-28
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Comparative reverse transcription-polymerase chain reaction and in situ hybridization analyses of human imprinted p57KIP2 and insulin-like growth factor 2 gene transcripts in fetal kidney and Wilms' tumors using archival tissue.
pubmed:affiliation
Department of Pathology, Dunedin School of Medicine, University of Otago, New Zealand.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't