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dc.contributor.authorLosi-Guembarovski, Roberta
dc.contributor.authorKuasne, Hellen
dc.contributor.authorGuembarovski, Alda L.
dc.contributor.authorRainho, Claudia A.
dc.contributor.authorColus, Ilce M. S.
dc.date.accessioned2014-05-20T13:50:09Z
dc.date.available2014-05-20T13:50:09Z
dc.date.issued2007-12-01
dc.identifierhttp://dx.doi.org/10.1016/j.cancergencyto.2007.05.029
dc.identifier.citationCancer Genetics and Cytogenetics. New York: Elsevier B.V., v. 179, n. 2, p. 140-145, 2007.
dc.identifier.issn0165-4608
dc.identifier.urihttp://hdl.handle.net/11449/17900
dc.description.abstractGenetic and epigenetic alterations in choroid plexus tumors, a rare neuroepithelial neoplasm most frequently detected in children, are poorly characterized. Epigenetic silencing associated with aberrant CpG island methylation is one mechanism leading to the loss of tumor suppressor functions in cancer cells. Using methylation-specific polymerase chain reaction, the methylation patterns of the genes CDH1 (E-cadherin), RARB (retinoic acid receptor, beta), and SFN (stratifin; 14-3-3 sigma) were retrospectively investigated in eight choroid plexus tumors (five papillomas, two atypical papillomas, and one carcinoma), as well as in two normal cortexes obtained after autopsy from male individuals aged 6 months and 64 years. Among the six pediatric tumors, the mean age at diagnosis was 1.8 years old (range, 0.2-6) and the two adult tumors were detected in a 66-year-old man and a 45-year-old woman. A high frequency of hypermethylation was detected in CDH1 and SFN genes in tumoral and normal cortex tissues. Tumor-specific RARB hypermethylation was observed in four papillomas. Further studies are required to evaluate the role of aberrant methylation in choroid plexus tumor progression. (c) 2007 Elsevier B.V. All rights reserved.en
dc.format.extent140-145
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofCancer Genetics and Cytogenetics
dc.sourceWeb of Science
dc.titleDNA methylation patterns of the CDHI, RARB, and SFN genes in choroid plexus tumorsen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Estadual de Londrina (UEL)
dc.contributor.institutionUniversidade Federal do Paraná (UFPR)
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.description.affiliationUniv Estadual Londrina, Ctr Biol Sci, Dept Gen Biol, Londrina, PR, Brazil
dc.description.affiliationUniversidade Federal do Paraná (UFPF), Dept Genet, BR-80060000 Curitiba, Parana, Brazil
dc.description.affiliationUniv Estadual Londrina, Dept Appl Pathol, Londrina, PR USA
dc.description.affiliationSão Paulo State Univ, UNESP, Biosci Inst, Dept Genet, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, UNESP, Biosci Inst, Dept Genet, BR-18618000 Botucatu, SP, Brazil
dc.identifier.doi10.1016/j.cancergencyto.2007.05.029
dc.identifier.wosWOS:000251478000009
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt
unesp.author.orcid0000-0002-0285-1162[4]
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