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Article: Altered E-cadherin expression and p120 catenin localization in esophageal squamous cell carcinoma
Title | Altered E-cadherin expression and p120 catenin localization in esophageal squamous cell carcinoma |
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Authors | |
Keywords | E-cadherin Esophageal squamous cell carcinoma (ESCC) Immunohistochemistry p120 Catenin Tumor differentiation |
Issue Date | 2007 |
Publisher | Springer 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? |
Abstract | Background: 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 Identifier | http://hdl.handle.net/10722/129391 |
ISSN | 2023 Impact Factor: 3.4 2023 SCImago Journal Rankings: 1.037 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Chung, Y | en_HK |
dc.contributor.author | Lam, AKY | en_HK |
dc.contributor.author | Luk, JM | en_HK |
dc.contributor.author | Law, S | en_HK |
dc.contributor.author | Chan, KW | en_HK |
dc.contributor.author | Lee, PY | en_HK |
dc.contributor.author | Wong, J | en_HK |
dc.date.accessioned | 2010-12-23T08:36:41Z | - |
dc.date.available | 2010-12-23T08:36:41Z | - |
dc.date.issued | 2007 | en_HK |
dc.identifier.citation | Annals Of Surgical Oncology, 2007, v. 14 n. 11, p. 3260-3267 | en_HK |
dc.identifier.issn | 1068-9265 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/129391 | - |
dc.description.abstract | Background: 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.language | eng | en_US |
dc.publisher | Springer New York LLC. The Journal's web site is located at http://www.annalssurgicaloncology.org | en_HK |
dc.relation.ispartof | Annals of Surgical Oncology | en_HK |
dc.rights | The original publication is available at www.springerlink.com | - |
dc.subject | E-cadherin | en_HK |
dc.subject | Esophageal squamous cell carcinoma (ESCC) | en_HK |
dc.subject | Immunohistochemistry | en_HK |
dc.subject | p120 Catenin | en_HK |
dc.subject | Tumor differentiation | en_HK |
dc.subject.mesh | Cadherins - metabolism | - |
dc.subject.mesh | Carcinoma, Squamous Cell - metabolism | - |
dc.subject.mesh | Cell Adhesion Molecules - metabolism | - |
dc.subject.mesh | Cell Membrane - metabolism | - |
dc.subject.mesh | Cytoplasm - metabolism | - |
dc.title | Altered E-cadherin expression and p120 catenin localization in esophageal squamous cell carcinoma | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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.email | Luk, JM: jmluk@hkucc.hku.hk | en_HK |
dc.identifier.email | Law, S: slaw@hku.hk | en_HK |
dc.identifier.email | Chan, KW: hrmtckw@hku.hk | en_HK |
dc.identifier.email | Wong, J: jwong@hkucc.hku.hk | en_HK |
dc.identifier.authority | Luk, JM=rp00349 | en_HK |
dc.identifier.authority | Law, S=rp00437 | en_HK |
dc.identifier.authority | Chan, KW=rp00330 | en_HK |
dc.identifier.authority | Wong, J=rp00322 | en_HK |
dc.description.nature | postprint | - |
dc.identifier.doi | 10.1245/s10434-007-9511-8 | en_HK |
dc.identifier.pmid | 17647062 | - |
dc.identifier.scopus | eid_2-s2.0-35348863666 | en_HK |
dc.identifier.hkuros | 137106 | en_US |
dc.identifier.hkuros | 138783 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-35348863666&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 14 | en_HK |
dc.identifier.issue | 11 | en_HK |
dc.identifier.spage | 3260 | en_HK |
dc.identifier.epage | 3267 | en_HK |
dc.identifier.eissn | 1534-4681 | - |
dc.identifier.isi | WOS:000250204500032 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Chung, Y=22833625500 | en_HK |
dc.identifier.scopusauthorid | Lam, AKY=7403657165 | en_HK |
dc.identifier.scopusauthorid | Luk, JM=7006777791 | en_HK |
dc.identifier.scopusauthorid | Law, S=7202241293 | en_HK |
dc.identifier.scopusauthorid | Chan, KW=16444133100 | en_HK |
dc.identifier.scopusauthorid | Lee, PY=8731985700 | en_HK |
dc.identifier.scopusauthorid | Wong, J=8049324500 | en_HK |
dc.identifier.issnl | 1068-9265 | - |