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Article: Altered E-cadherin expression and p120 catenin localization in esophageal squamous cell carcinoma

TitleAltered E-cadherin expression and p120 catenin localization in esophageal squamous cell carcinoma
Authors
KeywordsE-cadherin
Esophageal squamous cell carcinoma (ESCC)
Immunohistochemistry
p120 Catenin
Tumor differentiation
Issue Date2007
PublisherSpringer New York LLC. The Journal's web site is located at http://www.annalssurgicaloncology.org
Citation
Annals Of Surgical Oncology, 2007, v. 14 n. 11, p. 3260-3267 How to Cite?
AbstractBackground: E-cadherin is a well-known tumor suppressor and its dysregulated expression correlates with tumor differentiation, metastasis and survival in esophageal squamous cell carcinoma (ESCC). p120 catenin is an Armadillo protein normally bound to E-cadherin in the cadherin-catenin complex at the adherens junction. Dysregulated expression and mislocalization of p120ctn affect the protective function of the complex. The objective of the present study was to evaluate the clinical significance of E-cadherin and p120ctn expression in ESCC. Methods: Immunohistochemistry was performed to investigate the expression of E-cadherin and p120ctn proteins in 71 patients with ESCC. The relationships between protein expression and clinicopathological characteristics were analyzed. Results: Reduced E-cadherin and p120ctn expressions were observed in 42.3% and 8.5% of ESCC cases, respectively. Reduction of membranous p120ctn was observed in 33.8% of cases. Membranous E-cadherin was preserved when p120ctn co-localized on the membrane of tumor cells (72.3%, P = 0.001). High level E-cadherin expression and membranous p120ctn preservation positively correlated with tumor differentiation (P = 0.001 and P = 0.008, respectively). p120ctn expression was also significantly related to lymph node metastasis (P = 0.003). Heterogeneous expression of both E-cadherin and p120ctn was observed in dysplasia. Conclusions: Altered E-cadherin expression and p120ctn localization were related to tumor differentiation, indicating their important roles in the pathogenesis of ESCC. © 2007 The Society of Surgical Oncology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/129391
ISSN
2015 Impact Factor: 3.655
2015 SCImago Journal Rankings: 1.902
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChung, Yen_HK
dc.contributor.authorLam, AKYen_HK
dc.contributor.authorLuk, JMen_HK
dc.contributor.authorLaw, Sen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorLee, PYen_HK
dc.contributor.authorWong, Jen_HK
dc.date.accessioned2010-12-23T08:36:41Z-
dc.date.available2010-12-23T08:36:41Z-
dc.date.issued2007en_HK
dc.identifier.citationAnnals Of Surgical Oncology, 2007, v. 14 n. 11, p. 3260-3267en_HK
dc.identifier.issn1068-9265en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129391-
dc.description.abstractBackground: E-cadherin is a well-known tumor suppressor and its dysregulated expression correlates with tumor differentiation, metastasis and survival in esophageal squamous cell carcinoma (ESCC). p120 catenin is an Armadillo protein normally bound to E-cadherin in the cadherin-catenin complex at the adherens junction. Dysregulated expression and mislocalization of p120ctn affect the protective function of the complex. The objective of the present study was to evaluate the clinical significance of E-cadherin and p120ctn expression in ESCC. Methods: Immunohistochemistry was performed to investigate the expression of E-cadherin and p120ctn proteins in 71 patients with ESCC. The relationships between protein expression and clinicopathological characteristics were analyzed. Results: Reduced E-cadherin and p120ctn expressions were observed in 42.3% and 8.5% of ESCC cases, respectively. Reduction of membranous p120ctn was observed in 33.8% of cases. Membranous E-cadherin was preserved when p120ctn co-localized on the membrane of tumor cells (72.3%, P = 0.001). High level E-cadherin expression and membranous p120ctn preservation positively correlated with tumor differentiation (P = 0.001 and P = 0.008, respectively). p120ctn expression was also significantly related to lymph node metastasis (P = 0.003). Heterogeneous expression of both E-cadherin and p120ctn was observed in dysplasia. Conclusions: Altered E-cadherin expression and p120ctn localization were related to tumor differentiation, indicating their important roles in the pathogenesis of ESCC. © 2007 The Society of Surgical Oncology, Inc.en_HK
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://www.annalssurgicaloncology.orgen_HK
dc.relation.ispartofAnnals of Surgical Oncologyen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectE-cadherinen_HK
dc.subjectEsophageal squamous cell carcinoma (ESCC)en_HK
dc.subjectImmunohistochemistryen_HK
dc.subjectp120 Cateninen_HK
dc.subjectTumor differentiationen_HK
dc.subject.meshCadherins - metabolism-
dc.subject.meshCarcinoma, Squamous Cell - metabolism-
dc.subject.meshCell Adhesion Molecules - metabolism-
dc.subject.meshCell Membrane - metabolism-
dc.subject.meshCytoplasm - metabolism-
dc.titleAltered E-cadherin expression and p120 catenin localization in esophageal squamous cell carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1068-9265&volume=14&issue=11&spage=3260&epage=3267&date=2007&atitle=Altered+E-cadherin+expression+and+p120+catenin+localization+in+esophageal+squamous+cell+carcinoma-
dc.identifier.emailLuk, JM: jmluk@hkucc.hku.hken_HK
dc.identifier.emailLaw, S: slaw@hku.hken_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailWong, J: jwong@hkucc.hku.hken_HK
dc.identifier.authorityLuk, JM=rp00349en_HK
dc.identifier.authorityLaw, S=rp00437en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityWong, J=rp00322en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1245/s10434-007-9511-8en_HK
dc.identifier.pmid17647062-
dc.identifier.scopuseid_2-s2.0-35348863666en_HK
dc.identifier.hkuros137106en_US
dc.identifier.hkuros138783-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35348863666&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue11en_HK
dc.identifier.spage3260en_HK
dc.identifier.epage3267en_HK
dc.identifier.eissn1534-4681-
dc.identifier.isiWOS:000250204500032-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChung, Y=22833625500en_HK
dc.identifier.scopusauthoridLam, AKY=7403657165en_HK
dc.identifier.scopusauthoridLuk, JM=7006777791en_HK
dc.identifier.scopusauthoridLaw, S=7202241293en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridLee, PY=8731985700en_HK
dc.identifier.scopusauthoridWong, J=8049324500en_HK

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