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dc.creatorLázcoz, Paulaes_ES
dc.creatorMuñoz, Jorgees_ES
dc.creatorNistal, Manueles_ES
dc.creatorPestaña, Ángeles_ES
dc.creatorEncío Martínez, Ignacioes_ES
dc.creatorSáez Castresana, Javieres_ES
dc.date.accessioned2014-06-04T11:15:10Z
dc.date.available2014-06-04T11:15:10Z
dc.date.issued2006
dc.identifier.issn1471-2407
dc.identifier.other819
dc.identifier.urihttps://hdl.handle.net/2454/10723
dc.description.abstractBackground: Epigenetic alterations and loss of heterozygosity are mechanisms of tumor suppressor gene inactivation. A new carcinogenic pathway, targeting the RAS effectors has recently been documented. RASSF1A, on 3p21.3, and NORE1A, on 1q32.1, are among the most important, representative RAS effectors. Methods: We screened the 3p21 locus for the loss of heterozygosity and the hypermethylation status of RASSF1A, NORE1A and BLU ( the latter located at 3p21.3) in 41 neuroblastic tumors. The statistical relationship of these data was correlated with CASP8 hypermethylation. The expression levels of these genes, in cell lines, were analyzed by RT-PCR. Results: Loss of heterozygosity and microsatellite instability at 3p21 were detected in 14% of the analyzed tumors. Methylation was different for tumors and cell lines (tumors: 83% in RASSF1A, 3% in NORE1A, 8% in BLU and 60% in CASP8; cell lines: 100% in RASSF1A, 50% in NORE1A, 66% in BLU and 92% in CASP8). In cell lines, a correlation with lack of expression was evident for RASSF1A, but less clear for NORE1A, BLU and CASP8. We could only demonstrate a statistically significant association between hypermethylation of RASSF1A and hypermethylation of CASP8, while no association with MYCN amplification, 1p deletion, and/or aggressive histological pattern of the tumor was demonstrated. Conclusion: 1) LOH at 3p21 appears in a small percentage of neuroblastomas, indicating that a candidate tumor suppressor gene of neuroblastic tumors is not located in this region. 2) Promoter hypermethylation of RASSF1A and CASP8 occurs at a high frequency in neuroblastomas.en
dc.description.sponsorshipThis research was supported in part by grants from the Departamentos de Salud y de Educación del Gobierno de Navarra, Pamplona; Fondo de Investigación Sanitaria (PI031356), and Ministerio de Ciencia y Tecnología y Fondo Europeo de Desarrollo Regional (BFI2003-08775), Madrid.en
dc.format.mimetypeapplication/pdfen
dc.language.isoengen
dc.publisherBioMed Centralen
dc.relation.ispartofBMC Cancer, 2006, 6: 254en
dc.rights© 2006 Lázcoz et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/
dc.subjectTumor suppressor geneen
dc.subjectHuman chromosome 3P21.3en
dc.subjectRenal cell carcinomaen
dc.subjectCPG islanden
dc.subjectEpigenetic inactivationen
dc.subjectCaspase 8 geneen
dc.subjectMethylationen
dc.subjectAnalysisen
dc.subjectMYCN amplificationen
dc.subjectPediatric tumorsen
dc.subjectHuman cancersen
dc.subjectOncologyen
dc.titleFrequent promoter hypermethylation of RASSF1A and CASP8 in neuroblastomaen
dc.typeArtículo / Artikuluaes
dc.typeinfo:eu-repo/semantics/articleen
dc.contributor.departmentUniversidad Pública de Navarra. Departamento de Ciencias de la Saludes_ES
dc.contributor.departmentNafarroako Unibertsitate Publikoa. Osasun Zientziak Sailaeu
dc.rights.accessRightsAcceso abierto / Sarbide irekiaes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen
dc.identifier.doi10.1186/1471-2407-6-254
dc.relation.publisherversionhttps://dx.doi.org/10.1186/1471-2407-6-254
dc.type.versionVersión publicada / Argitaratu den bertsioaes
dc.type.versioninfo:eu-repo/semantics/publishedVersionen


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© 2006 Lázcoz et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as © 2006 Lázcoz et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.