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dc.creatorMartín Sánchez, Esperanzaes_ES
dc.creatorMendaza Lainez, Saioaes_ES
dc.creatorUlazia Garmendia, Anees_ES
dc.creatorMonreal Santesteban, Iñakies_ES
dc.creatorCórdoba Iturriagagoitia, Aliciaes_ES
dc.creatorVicente García, Franciscoes_ES
dc.creatorBlanco Luquin, Idoiaes_ES
dc.creatorCruz, Susana de laes_ES
dc.creatorAramendia, Anaes_ES
dc.creatorGuerrero, Davides_ES
dc.date.accessioned2018-10-23T07:35:33Z
dc.date.available2018-10-23T07:35:33Z
dc.date.issued2017
dc.identifier.issn1868-7075 (Print)
dc.identifier.issn1868-7083 (Electronic)
dc.identifier.urihttps://hdl.handle.net/2454/31121
dc.description.abstractBackground: Cadherin-like protein 22 (CDH22) is a transmembrane glycoprotein involved in cell-cell adhesion and metastasis. Its role in cancer is controversial because it has been described as being upregulated in colorectal cancer, whereas it is downregulated in metastatic melanoma. However, its status in breast cancer (BC) is unknown. The purpose of our study was to determine the molecular status and clinical value of CDH22 in BC. Results: We observed by immunohistochemistry that the level of CDH22 expression was lower in BC tissues than in their matched adjacent-to-tumour and non-neoplastic tissues from reduction mammoplasties. Since epigenetic alteration is one of the main causes of gene silencing, we analysed the hypermethylation of 3 CpG sites in the CDH22 promoter by pyrosequencing in a series of 142 infiltrating duct BC cases. CDH22 was found to be hypermethylated in tumoral tissues relative to non-neoplastic mammary tissues. Importantly, this epigenetic alteration was already present in adjacent-to-tumour tissues, although to a lesser extent than in tumoral samples. Furthermore, CDH22 gene regulation was dynamically modulated in vitro by epigenetic drugs. Interestingly, CDH22 hypermethylation in all 3 CpG sites simultaneously, but not expression, was significantly associated with shorter progression-free survival (p = 0.015) and overall survival (p = 0.021) in our patient series. Importantly, CDH22 hypermethylation was an independent factor that predicts poor progression-free survival regardless of age and stage (p = 0.006). Conclusions: Our results are the first evidence that CDH22 is hypermethylated in BC and that this alteration is an independent prognostic factor in BC. Thus, CDH22 hypermethylation could be a potential biomarker of poor prognosis in BC.en
dc.description.sponsorshipThis work has been funded in competitive calls by the Spanish Institute of Health (PI14/00579), the Basque Foundation for Healthcare Research and Innovation (BIO-11-CM-013), La Caixa Foundation (70789) and the Breast Cancer Patients’ Association in Navarra (SARAY). EMS is the recipient of a grant from the Spanish Ministry of Economy and Competitiveness (PTA2015-11895-I).en
dc.format.extent8 p.
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherBioMed Centralen
dc.relation.ispartofClinical Epigenetics (2017) 9:7en
dc.rights© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stateden
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectCDH22en
dc.subjectDNA methylationen
dc.subjectBreast canceren
dc.subjectPredictive biomarkeren
dc.titleCDH22 hypermethylation is an independent prognostic biomarker in breast canceren
dc.typeinfo:eu-repo/semantics/articleen
dc.typeArtículo / Artikuluaes
dc.contributor.departmentUniversidad Pública de Navarra. Departamento de Ciencias de la Saludes_ES
dc.contributor.departmentNafarroako Unibertsitate Publikoa. Osasun Zientziak Sailaeu
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen
dc.rights.accessRightsAcceso abierto / Sarbide irekiaes
dc.identifier.doi10.1186/s13148-016-0309-z
dc.relation.publisherversionhttps://doi.org/10.1186/s13148-016-0309-z
dc.type.versioninfo:eu-repo/semantics/publishedVersionen
dc.type.versionVersión publicada / Argitaratu den bertsioaes


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© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License, which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated
La licencia del ítem se describe como © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated