2.50
Hdl Handle:
http://hdl.handle.net/2336/32953
Title:
Alterations of E-cadherin and beta-catenin in gastric cancer
Authors:
Huiping, C; Kristjansdottir, S; Jonasson, JG; Magnusson, J; Egilsson, V; Ingvarsson, S
Citation:
BMC Cancer. 2001;1:16
Issue Date:
29-Oct-2001
Abstract:
BACKGROUND: The E-cadherin-catenin complex plays a crucial role in epithelial cell-cell adhesion and in the maintenance of tissue architecture. Perturbation in the expression or function of this complex results in loss of intercellular adhesion, with possible consequent cell transformation and tumour progression. METHODS: We studied the alterations of E-cadherin and beta-catenin in a set of 50 primary gastric tumours by using loss of heterozygosity (LOH) analysis, gene mutation screening, detection of aberrant transcripts and immunohistochemistry (IHC). RESULTS: A high frequency (75%) of LOH was detected at 16q22.1 containing E-cadherin locus. Three cases (6%) showed the identical missense mutation, A592T. This mutation is not likely to contribute strongly to the carcinogenesis of gastric cancer, because a low frequency (1.6%) of this mutation was also found in 187 normal individuals. We also detected a low frequency (0.36%, 0%) of this mutation in 280 breast tumours and 444 other tumours, including colon and rectum, lung, endometrium, ovary, testis, kidney, thyroid carcinomas and sarcomas, respectively. We also analyzed the aberrant E-cadherin mRNAs in the gastric tumours and found that 7 tumours (18%) had aberrant mRNAs in addition to the normal mRNA. These aberrant mRNAs may produce abnormal E-cadherin molecules, resulting in weak cell-cell adhesion and invasive behaviour of carcinoma cells. Reduced expression of E-cadherin and beta-catenin was identified at the frequency of 42% and 28%, respectively. Specially, 11 tumours (22%) exhibited positive cytoplasmic staining for beta-catenin IHC. An association was found between reduced expression of E-cadherin and beta-catenin. Moreover, an association was detected between reduced expression of E-cadherin and diffuse histotype. CONCLUSION: Our results support the hypothesis that alterations of E-cadherin and beta-catenin play a role in the initiation and progression of gastric cancer.
Description:
To access full text version of this article. Please click on the hyperlink "View/Open" at the bottom of this page

Full metadata record

DC FieldValue Language
dc.contributor.authorHuiping, C-
dc.contributor.authorKristjansdottir, S-
dc.contributor.authorJonasson, JG-
dc.contributor.authorMagnusson, J-
dc.contributor.authorEgilsson, V-
dc.contributor.authorIngvarsson, S-
dc.date.accessioned2008-07-24T09:38:12Z-
dc.date.available2008-07-24T09:38:12Z-
dc.date.issued2001-10-29-
dc.date.submitted2008-07-24-
dc.identifier.citationBMC Cancer. 2001;1:16en
dc.identifier.issn1471-2407-
dc.identifier.pmid11747475-
dc.identifier.doi10.1186/1471-2407-1-16-
dc.identifier.urihttp://hdl.handle.net/2336/32953-
dc.descriptionTo access full text version of this article. Please click on the hyperlink "View/Open" at the bottom of this pageen
dc.description.abstractBACKGROUND: The E-cadherin-catenin complex plays a crucial role in epithelial cell-cell adhesion and in the maintenance of tissue architecture. Perturbation in the expression or function of this complex results in loss of intercellular adhesion, with possible consequent cell transformation and tumour progression. METHODS: We studied the alterations of E-cadherin and beta-catenin in a set of 50 primary gastric tumours by using loss of heterozygosity (LOH) analysis, gene mutation screening, detection of aberrant transcripts and immunohistochemistry (IHC). RESULTS: A high frequency (75%) of LOH was detected at 16q22.1 containing E-cadherin locus. Three cases (6%) showed the identical missense mutation, A592T. This mutation is not likely to contribute strongly to the carcinogenesis of gastric cancer, because a low frequency (1.6%) of this mutation was also found in 187 normal individuals. We also detected a low frequency (0.36%, 0%) of this mutation in 280 breast tumours and 444 other tumours, including colon and rectum, lung, endometrium, ovary, testis, kidney, thyroid carcinomas and sarcomas, respectively. We also analyzed the aberrant E-cadherin mRNAs in the gastric tumours and found that 7 tumours (18%) had aberrant mRNAs in addition to the normal mRNA. These aberrant mRNAs may produce abnormal E-cadherin molecules, resulting in weak cell-cell adhesion and invasive behaviour of carcinoma cells. Reduced expression of E-cadherin and beta-catenin was identified at the frequency of 42% and 28%, respectively. Specially, 11 tumours (22%) exhibited positive cytoplasmic staining for beta-catenin IHC. An association was found between reduced expression of E-cadherin and beta-catenin. Moreover, an association was detected between reduced expression of E-cadherin and diffuse histotype. CONCLUSION: Our results support the hypothesis that alterations of E-cadherin and beta-catenin play a role in the initiation and progression of gastric cancer.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.subject.meshAge of Onseten
dc.subject.meshAgeden
dc.subject.meshBreast Neoplasmsen
dc.subject.meshCadherinsen
dc.subject.meshCell Adhesionen
dc.subject.meshChromosomes, Human, Pair 16en
dc.subject.meshCytoskeletal Proteinsen
dc.subject.meshDNA Mutational Analysisen
dc.subject.meshDNA, Neoplasmen
dc.subject.meshFemaleen
dc.subject.meshGene Expression Regulation, Neoplasticen
dc.subject.meshGerm-Line Mutationen
dc.subject.meshHumansen
dc.subject.meshLoss of Heterozygosityen
dc.subject.meshMaleen
dc.subject.meshMutation, Missenseen
dc.subject.meshProstatic Neoplasmsen
dc.subject.meshSkin Neoplasmsen
dc.subject.meshStomach Neoplasmsen
dc.subject.meshTrans-Activatorsen
dc.subject.meshbeta Cateninen
dc.titleAlterations of E-cadherin and beta-catenin in gastric canceren
dc.typeArticleen
dc.contributor.departmentDepartment of Pathology, National University Hospital, 101 Reykjavík, Iceland. chen@rsp.isen
dc.identifier.journalBMC canceren

Related articles on PubMed

All Items in Hirsla are protected by copyright, with all rights reserved, unless otherwise indicated.