Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-6-15
pubmed:abstractText
The activation of the adenomatous polyposis coli (APC)/beta-catenin/T-cell factor (Tcf) pathway due to beta-catenin gene mutation has been recently implicated in the development of some endometrial carcinomas. beta- and gamma-catenin are structurally and functionally related molecules that participate in cell adhesion and signal transduction. Nuclear accumulation of beta- and gamma-catenin have been related to the activation of the APC/beta-catenin/Tcf pathway. In this study, we investigate the immunohistochemical expression pattern (nuclear vs membranous) of beta- and gamma-catenin in 40 endometrial carcinomas and their correlation with clinicopathological features and microsatellite instability (MI) status. MI was detected at three or more loci in 12 tumors: 11 were endometrioid and one was non-endometrioid. Nuclear catenin expression was found in 13 carcinomas: ten carcinomas had nuclear beta-catenin expression and three carcinomas had nuclear gamma-catenin expression. The nuclear catenin expression pattern significantly correlated with the histological type, International Federation of Gynecology and Obstetrics (FIGO) grade, and the presence of a second neoplasm. Nuclear catenin expression was always observed in low-grade endometrioid carcinomas; it was also more frequently associated with a second carcinoma. No correlation was observed between the catenin expression pattern and the level of myometrial infiltration, stage, associated endometrial hyperplasia, the existence of a source of estrogenic stimulation, and MI. However, four of 13 endometrioid carcinomas in this series had both catenin nuclear expression and MI. These data suggest that at least two different neoplastic pathways can lead to endometrial carcinomas with an endometrioid phenotype. In one, MI would be a key event, while in the other, the APC/beta-catenin/Tcf signaling pathways could be activated. Probably, in some cases, both pathways could simultaneously occur.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0945-6317
pubmed:author
pubmed:issnType
Print
pubmed:volume
438
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
464-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11407474-Carcinoma, Endometrioid, pubmed-meshheading:11407474-Cell Nucleus, pubmed-meshheading:11407474-Cytoskeletal Proteins, pubmed-meshheading:11407474-DNA, Neoplasm, pubmed-meshheading:11407474-Desmoplakins, pubmed-meshheading:11407474-Endometrial Neoplasms, pubmed-meshheading:11407474-Female, pubmed-meshheading:11407474-Gene Expression Regulation, Neoplastic, pubmed-meshheading:11407474-Humans, pubmed-meshheading:11407474-Immunoenzyme Techniques, pubmed-meshheading:11407474-Intracellular Membranes, pubmed-meshheading:11407474-Microsatellite Repeats, pubmed-meshheading:11407474-Neoplasm Staging, pubmed-meshheading:11407474-Polymerase Chain Reaction, pubmed-meshheading:11407474-Trans-Activators, pubmed-meshheading:11407474-beta Catenin, pubmed-meshheading:11407474-gamma Catenin
pubmed:year
2001
pubmed:articleTitle
Beta- and gamma-catenin expression in endometrial carcinoma. Relationship with clinicopathological features and microsatellite instability.
pubmed:affiliation
Programa de Patología Molecular, Centro Nacional de Investigaciones Oncológicas Carlos III, Madrid, Spain. jpalacios@cnio.es
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't