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dc.contributor.authorBermudo, Raquel-
dc.contributor.authorAbia, David-
dc.contributor.authorFerrer, Berta-
dc.contributor.authorNayach, Iracema-
dc.contributor.authorBenguria, Alberto-
dc.contributor.authorZaballos, Ángel-
dc.contributor.authorRey, Javier del-
dc.contributor.authorMiró, Rosa-
dc.contributor.authorCampo, Elías-
dc.contributor.authorMartínez-Alonso, Carlos-
dc.contributor.authorRamírez Ortiz, Miguel Ángel-
dc.contributor.authorFernández, Pedro L.-
dc.contributor.authorThomson, Timothy M.-
dc.date.accessioned2008-12-30T09:51:17Z-
dc.date.available2008-12-30T09:51:17Z-
dc.date.issued2008-10-30-
dc.identifier.citationBMC Cancer 2008, 8:315en_US
dc.identifier.issn1471-2407-
dc.identifier.urihttp://hdl.handle.net/10261/9400-
dc.description12 pages, 4 figures.-- PMID: 18973659 [PubMed].-- PMCID: PMC2585097.-- Additional information available: File 1: Table showing FADA-selected genes information (58 pages).- File 2: Graphical representation of the genes selected by FADA (1 page).en_US
dc.descriptionThe authors wish to dedicate this report to the memory of the late Ángel R. Ortiz, a key contributor to this report.-
dc.description.abstract[Background] Transcriptional profiling of prostate cancer (PC) has unveiled new markers of neoplasia and allowed insights into mechanisms underlying this disease. Genomewide analyses have also identified new chromosomal abnormalities associated with PC. The combination of both classes of data for the same sample cohort might provide better criteria for identifying relevant factors involved in neoplasia. Here we describe transcriptional signatures identifying distinct normal and tumoral prostate tissue compartments, and the inference and demonstration of a new, highly recurrent copy number gain on chromosome 17q25.3.en_US
dc.description.abstract[Methods] We have applied transcriptional profiling to tumoral and non-tumoral prostate samples with relatively homogeneous epithelial representations as well as pure stromal tissue from peripheral prostate and cultured cell lines, followed by quantitative RT-PCR validations and immunohistochemical analysis. In addition, we have performed in silico colocalization analysis of coregulated genes and validation by fluorescent in situ hybridization (FISH).en_US
dc.description.abstract[Results] The transcriptomic analysis has allowed us to identify signatures corresponding to non-tumoral luminal and tumoral epithelium, basal epithelial cells, and prostate stromal tissue. In addition, in silico analysis of co-regulated expression of physically linked genes has allowed us to predict the occurrence of a copy number gain at chromosomal region 17q25.3. This computational inference was validated by fluorescent in situ hybridization, which showed gains in this region in over 65% of primary and metastatic tumoral samples.en_US
dc.description.abstract[Conclusion] Our approach permits to directly link gene copy number variations with transcript co-regulation in association with neoplastic states. Therefore, transcriptomic studies of carefully selected samples can unveil new diagnostic markers and transcriptional signatures highly specific of PC, and lead to the discovery of novel genomic abnormalities that may provide additional insights into the causes and mechanisms of prostate cancer.en_US
dc.description.sponsorshipThis study was supported by grants from the Ministerio de Educación (GEN2001-4856-C13, GEN2001-4865-C13-10 and SAF2005-05109), the Ministerio de Sanidad (PI020231), the Fundació Marató TV3, the Red Temática de Cáncer of the Instituto Carlos III (RET2039) and the Fundación Ramón Areces.en_US
dc.format.extent3480300 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherBioMed Centralen_US
dc.relation.isversionofPublisher’s version-
dc.rightsopenAccessen_US
dc.subjectProstate canceren_US
dc.subjectTranscriptional profilingen_US
dc.subjectMarkers of neoplasiaen_US
dc.subjectChromosomal abnormalitiesen_US
dc.subjectChromosome 17q25.3en_US
dc.subjectCopy number gainen_US
dc.subjectStromal tissueen_US
dc.subjectFluorescent in situ hybridization (FISH)en_US
dc.titleCo-regulation analysis of closely linked genes identifies a highly recurrent gain on chromosome 17q25.3 in prostate canceren_US
dc.typeartículoen_US
dc.identifier.doi10.1186/1471-2407-8-315-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1186/1471-2407-8-315en_US
dc.contributor.funderMinisterio de Educación (España)-
dc.contributor.funderMinisterio de Sanidad y Consumo (España)-
dc.contributor.funderFundació La Marató de TV3-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderFundación Ramón Areces-
dc.identifier.funderhttp://dx.doi.org/10.13039/100008666es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100008054es_ES
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