rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
3
|
pubmed:dateCreated |
1999-10-7
|
pubmed:abstractText |
Inappropriate activation of the Wnt pathway resulting from beta-catenin gene alterations has recently been implicated in the development of hepatocellular carcinoma (HCC). To explore the in vivo effects of mutated beta-catenin, HCC specimens from 32 patients carrying one or several tumors were screened for somatic mutations in exon 3 of the beta-catenin gene, and the expression and subcellular localization of beta-catenin was studied by immunohistochemistry. Missense mutations or interstitial deletions in beta-catenin exon 3 were detected in 12 of 35 (34%) HCC samples. After immunostaining, most tumors exhibited increased membranous and/or cytoplasmic expression of beta-catenin compared with adjacent nontumoral liver. Strong nuclear accumulation of beta-catenin was observed either focally or uniformly in 15 of 35 (43%) tumor specimens, but not in cirrhotic nodules or dysplastic liver cells in adjacent liver. Aberrant nuclear expression of beta-catenin was significantly associated with the presence of mutations in the beta-catenin gene (P < 0.005). Moreover, nuclear beta-catenin staining correlated significantly with increased Ki-67 proliferative index in tumor (P < 0.001) and seemed to be associated with poor outcome in patients with HCC. In conclusion, our data indicate that activation of the Wnt/beta-catenin pathway in HCC results mainly from somatic mutations in the beta-catenin gene and may promote tumor progression by stimulating tumor cell proliferation.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-10027390,
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0002-9440
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
155
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
703-10
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:10487827-Adult,
pubmed-meshheading:10487827-Aged,
pubmed-meshheading:10487827-Amino Acid Sequence,
pubmed-meshheading:10487827-Carcinoma, Hepatocellular,
pubmed-meshheading:10487827-Cell Division,
pubmed-meshheading:10487827-Cell Nucleus,
pubmed-meshheading:10487827-Cytoskeletal Proteins,
pubmed-meshheading:10487827-DNA Mutational Analysis,
pubmed-meshheading:10487827-Female,
pubmed-meshheading:10487827-Humans,
pubmed-meshheading:10487827-Immunohistochemistry,
pubmed-meshheading:10487827-Ki-67 Antigen,
pubmed-meshheading:10487827-Liver Neoplasms,
pubmed-meshheading:10487827-Male,
pubmed-meshheading:10487827-Middle Aged,
pubmed-meshheading:10487827-Mitotic Index,
pubmed-meshheading:10487827-Mutation,
pubmed-meshheading:10487827-Polymerase Chain Reaction,
pubmed-meshheading:10487827-Recurrence,
pubmed-meshheading:10487827-Survival Rate,
pubmed-meshheading:10487827-Trans-Activators,
pubmed-meshheading:10487827-beta Catenin
|
pubmed:year |
1999
|
pubmed:articleTitle |
Nuclear accumulation of mutated beta-catenin in hepatocellular carcinoma is associated with increased cell proliferation.
|
pubmed:affiliation |
Département de Pathologie, Service de Chirurgie, Hôpital Henri Mondor - AP-HP, Créteil, Paris, France.
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pubmed:publicationType |
Journal Article
|