Statements in which the resource exists as a subject.
PredicateObject
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.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-10027390, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-10072352, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-10201372, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-10398104, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-1655254, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-7493029, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-7506118, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8103417, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8205525, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8402727, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8616874, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8638126, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8675162, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-8806074, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9065402, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9142060, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9196022, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9205099, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9370957, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9407023, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9433138, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9500465, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9537226, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9635571, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9635572, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9671767, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9707618, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9721853, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9727977, http://linkedlifedata.com/resource/pubmed/commentcorrection/10487827-9843955
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.
pubmed:publicationType
Journal Article