Source:http://linkedlifedata.com/resource/pubmed/id/11012986
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
2000-11-6
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| pubmed:abstractText |
beta-Catenin acts as a downstream transcriptional activator of the Wingless-Wnt signaling pathway. The beta-catenin-Tcf complex transactivates the downstream genes that regulate cell proliferation or inhibit apoptosis. The activation of this pathway through stabilization of beta-catenin is caused either by inactivating mutations of adenomatous polyposis coli (APC) tumor suppressor gene or by activating mutations in beta-catenin exon 3. To determine whether the abnormal expression and activating mutations in exon 3 of the beta-catenin gene are implicated in renal cell carcinogenesis, 52 renal cell carcinomas (RCC) were analyzed by immunohistochemistry, polymerase chain reaction-single-strand conformational polymorphism analysis (PCR-SSCP), and direct DNA sequencing. Immunohistochemically, all cases, as well as normal kidneys, showed membranous and/or cytoplasmic staining patterns without nuclear localization. However, the cytoplasmic accumulations of beta-catenin were observed in five (22.7%) of 22 cases of conventional (clear cell) renal carcinoma, but not in papillary or chromophobe renal carcinomas. The beta-catenin mutation was identified in only one case of conventional renal carcinoma and was a single-base missense mutation on codon 61, leading to substitution of glutamine by arginine. In conclusion, this study demonstrates that beta-catenin mutations are a relatively rare event in RCC and that cytoplasmic accumulations of beta-catenin protein are found only in conventional (clear cell) renal carcinomas. These data suggest that the activation of the beta-catenin signaling pathway may partly play a role in the development of conventional RCC.
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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/CTNNB1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cytoskeletal Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Neoplasm,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
1320-5463
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
50
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
725-30
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| pubmed:dateRevised |
2005-11-17
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| pubmed:meshHeading |
pubmed-meshheading:11012986-Adenocarcinoma,
pubmed-meshheading:11012986-Adult,
pubmed-meshheading:11012986-Aged,
pubmed-meshheading:11012986-Carcinoma, Papillary,
pubmed-meshheading:11012986-Carcinoma, Renal Cell,
pubmed-meshheading:11012986-Cytoskeletal Proteins,
pubmed-meshheading:11012986-DNA, Neoplasm,
pubmed-meshheading:11012986-DNA Mutational Analysis,
pubmed-meshheading:11012986-DNA Primers,
pubmed-meshheading:11012986-Female,
pubmed-meshheading:11012986-Humans,
pubmed-meshheading:11012986-Immunoenzyme Techniques,
pubmed-meshheading:11012986-Kidney,
pubmed-meshheading:11012986-Kidney Neoplasms,
pubmed-meshheading:11012986-Male,
pubmed-meshheading:11012986-Middle Aged,
pubmed-meshheading:11012986-Mutation, Missense,
pubmed-meshheading:11012986-Neoplasm Staging,
pubmed-meshheading:11012986-Polymerase Chain Reaction,
pubmed-meshheading:11012986-Polymorphism, Single-Stranded Conformational,
pubmed-meshheading:11012986-Trans-Activators,
pubmed-meshheading:11012986-beta Catenin
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| pubmed:year |
2000
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| pubmed:articleTitle |
beta-catenin expression and mutational analysis in renal cell carcinomas.
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| pubmed:affiliation |
Department of Pathology, College of Medicine, Korea University, Gojan-Dong, Ansan, Korea. apysk@yahoo.com
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| pubmed:publicationType |
Journal Article
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