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Article: Loss of E-cadherin expression resulting from promoter hypermethylation in oral tongue carcinoma and its prognostic significance

TitleLoss of E-cadherin expression resulting from promoter hypermethylation in oral tongue carcinoma and its prognostic significance
Authors
Issue Date2002
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2002, v. 94 n. 2, p. 386-392 How to Cite?
AbstractBACKGROUND. E-cadherin is expressed on the surface of normal epithelial cells. Loss of E-cadherin expression has been found in cancers and is postulated to facilitate tumor cell dissociation and metastasis. This study evaluated the role of promoter dense methylation in the downregulation of E-cadherin expression in oral tongue carcinoma. METHODS. E-cadherin expression of 109 oral tongue carcinomas (93 primary tumors, 7 locally recurrent tumors, and 9 metastatic lymph nodes) was evaluated by immunohistochemical staining of tumor tissues. The methylation status of the CpG islands at the promoter region of E-cadherin which flanked five HpaII (methylation sensitive restriction enzyme) digestion sites were evaluated by methylation sensitive polymerase chain reaction in 86 tumors (70 primary tumors, 7 locally recurrent tumors, and 9 metastatic lymph nodes). RESULTS. Underexpression of E-cadherin was found in 83% of primary tumors, 86% of recurrent tumors, and 89% of nodal metastases, Hypermethylated E-cadherin promoter was found in 64% of primary tumors, 71% of recurrent tumors, and 67% of nodal metastases. Downregulation of E-cadherin expression was found to be related to promoter hypermethylation. Consistently weak expression of E-cadherin by promoter hypermethylation was observed in primary tumors, their corresponding metastatic lymph nodes, and recurrent tumors. Downregulation of E-cadherin expression was a significant poor prognostic factor for survival. CONCLUSIONS. Methylation of CpG sites at the promoter region played a key role in the inhibition of E-cadherin expression in both primary oral tongue carcinomas and their corresponding recurrences and nodal metastases. The resulting downregulation of E-cadherin expression had adverse effects on the prognosis of patients who were treated by primary surgery. © 2002 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/172812
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChang, HWen_US
dc.contributor.authorChow, Ven_US
dc.contributor.authorLam, KYen_US
dc.contributor.authorWei, WIen_US
dc.contributor.authorYuen, APWen_US
dc.date.accessioned2012-10-30T06:25:03Z-
dc.date.available2012-10-30T06:25:03Z-
dc.date.issued2002en_US
dc.identifier.citationCancer, 2002, v. 94 n. 2, p. 386-392en_US
dc.identifier.issn0008-543Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/172812-
dc.description.abstractBACKGROUND. E-cadherin is expressed on the surface of normal epithelial cells. Loss of E-cadherin expression has been found in cancers and is postulated to facilitate tumor cell dissociation and metastasis. This study evaluated the role of promoter dense methylation in the downregulation of E-cadherin expression in oral tongue carcinoma. METHODS. E-cadherin expression of 109 oral tongue carcinomas (93 primary tumors, 7 locally recurrent tumors, and 9 metastatic lymph nodes) was evaluated by immunohistochemical staining of tumor tissues. The methylation status of the CpG islands at the promoter region of E-cadherin which flanked five HpaII (methylation sensitive restriction enzyme) digestion sites were evaluated by methylation sensitive polymerase chain reaction in 86 tumors (70 primary tumors, 7 locally recurrent tumors, and 9 metastatic lymph nodes). RESULTS. Underexpression of E-cadherin was found in 83% of primary tumors, 86% of recurrent tumors, and 89% of nodal metastases, Hypermethylated E-cadherin promoter was found in 64% of primary tumors, 71% of recurrent tumors, and 67% of nodal metastases. Downregulation of E-cadherin expression was found to be related to promoter hypermethylation. Consistently weak expression of E-cadherin by promoter hypermethylation was observed in primary tumors, their corresponding metastatic lymph nodes, and recurrent tumors. Downregulation of E-cadherin expression was a significant poor prognostic factor for survival. CONCLUSIONS. Methylation of CpG sites at the promoter region played a key role in the inhibition of E-cadherin expression in both primary oral tongue carcinomas and their corresponding recurrences and nodal metastases. The resulting downregulation of E-cadherin expression had adverse effects on the prognosis of patients who were treated by primary surgery. © 2002 American Cancer Society.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_US
dc.relation.ispartofCanceren_US
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.-
dc.subject.meshCadherins - Genetics - Metabolismen_US
dc.subject.meshCarcinoma, Squamous Cell - Genetics - Metabolism - Pathologyen_US
dc.subject.meshCpg Islandsen_US
dc.subject.meshDna Methylationen_US
dc.subject.meshDna Primersen_US
dc.subject.meshDna, Neoplasm - Chemistryen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshLymphatic Metastasis - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshNeoplasm Recurrence, Localen_US
dc.subject.meshNeoplasm Stagingen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshPromoter Regions, Genetic - Geneticsen_US
dc.subject.meshTongue Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.titleLoss of E-cadherin expression resulting from promoter hypermethylation in oral tongue carcinoma and its prognostic significanceen_US
dc.typeArticleen_US
dc.identifier.emailWei, WI: hrmswwi@hku.hken_US
dc.identifier.authorityWei, WI=rp00323en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/cncr.10211en_US
dc.identifier.pmid11900224-
dc.identifier.scopuseid_2-s2.0-0037080420en_US
dc.identifier.hkuros72143-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037080420&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume94en_US
dc.identifier.issue2en_US
dc.identifier.spage386en_US
dc.identifier.epage392en_US
dc.identifier.isiWOS:000173303800013-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChang, HW=7407523249en_US
dc.identifier.scopusauthoridChow, V=7006616213en_US
dc.identifier.scopusauthoridLam, KY=7403657165en_US
dc.identifier.scopusauthoridWei, WI=7403321552en_US
dc.identifier.scopusauthoridWingYuen, AP=23104786200en_US

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