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dc.contributor.authorRodríguez-Rodero, Sandra-
dc.contributor.authorFernández, Agustín F.-
dc.contributor.authorFresno, Manuel-
dc.contributor.authorMancikova, Veronika-
dc.contributor.authorMendiola, Marta-
dc.contributor.authorHardisson, David-
dc.contributor.authorSantisteban, Pilar-
dc.contributor.authorRiesco-Eizaguirre, Garcilaso-
dc.contributor.authorMatías-Guiu, Xavier-
dc.contributor.authorCarnero, Amancio-
dc.contributor.authorRobledo, Mercedes-
dc.contributor.authorFraga, Mario F.-
dc.identifierdoi: 10.1210/jc.2012-3566-
dc.identifierissn: 0021-972X-
dc.identifiere-issn: 1945-7197-
dc.identifier.citationJournal of Clinical Endocrinology and Metabolism 98(7): 2811-2821 (2013)-
dc.descriptionet al.-
dc.description.abstract[Objective]: The purpose of this study was to determine the global patterns of aberrant DNA methylation in thyroid cancer. [Research Design and Methods]: We have used DNA methylation arrays to determine, for the first time, the genome-wide promoter methylation status of papillary, follicular, medullary, and anaplastic thyroid tumors. [Results]: We identified 262 and 352 hypermethylated and 13 and 21 hypomethylated genes in differentiated papillary and follicular tumors, respectively. Interestingly, the other tumor types analyzed displayed more hypomethylated genes (280 in anaplastic and 393 in medullary tumors) than aberrantly hypermethylated genes (86 in anaplastic and 131 in medullary tumors). Among the genes indentified, we show that 4 potential tumor suppressor genes (ADAMTS8, HOXB4, ZIC1, and KISS1R) and 4 potential oncogenes (INSL4, DPPA2, TCL1B, and NOTCH4) are frequently regulated by aberrant methylation in primary thyroid tumors. In addition, we show that aberrant promoter hypomethylation- associated overexpression of MAP17 might promote tumor growth in thyroid cancer. [Conclusions]: Thyroid cancer subtypes present differential promoter methylation signatures, and nondifferentiated subtypes are characterized by aberrant promoter hypomethylation rather than hypermethylation. Additional studies are needed to determine the potential clinical interest of the tumor subtype-specific DNA methylation signatures described herein and the role of aberrant promoter hypomethylation in nondifferentiated thyroid tumors. Copyright © 2013 by The Endocrine Society.-
dc.description.sponsorshipThis work has been financially supported by Fundación ASTURCOR(to S.R.R); the FIS/FEDER (PI11/01728 to A.F.F. and PI11/02795 to E.D.-A.); the ISCIII (CP11/00131 to A.F.F.); the FIS PI11/01359 to M.R.; the Spanish Ministry of Health (PS09/02454 and PI12/01080 to M.F.F.); the Spanish National Research Council (CSIC; 200820I172 to M.F.F.); Instituto Universitario de Oncología del Principado de Asturias (to C.F. and G.F.B.); Ramon Areces Foundation (to M.F.F. and G.F.B.); Fundacion Cientifica de la AECC (to R.G.U.); RD12/0036/0013, BFU-2010-16025, RD12/0036/0030 (to P.S.), RD12/0036/0015 and PI11/00929 (to C.S.), and S2011/BMD-2328 TIRONET (to P.S. and M.R.). Tumor samples were obtained with the support of Red de Biobancos ISCIII (RD09/0076/0059). V.M. is supported by a fellowship of “la Caixa”/Spanish National Cancer Research Center international PhD Program. The IUOPA is supported by the Obra Social Cajastur, Spain.-
dc.publisherEndocrine Society-
dc.titleDNA methylation signatures identify biologically distinct thyroid cancer subtypes-
dc.description.versionPeer Reviewed-
dc.contributor.funderComunidad de Madrid-
dc.contributor.funderFundación Asturcor-
dc.contributor.funderObra Social Cajastur-
dc.contributor.funderUniversidad de Oviedo-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderConsejo Superior de Investigaciones Científicas (España)-
dc.contributor.funderMinisterio de Sanidad, Servicios Sociales e Igualdad (España)-
dc.contributor.funderFundación Ramón Areces-
dc.contributor.funderFundación Científica Asociación Española Contra el Cáncer-
dc.contributor.funderLa Caixa-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
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