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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, Angel 
dc.contributor.authordel Rey, Javier
dc.contributor.authorMiró, Rosa
dc.contributor.authorCampo, Elías
dc.contributor.authorMartínez-A, Carlos
dc.contributor.authorOrtiz, Angel R
dc.contributor.authorFernández, Pedro L
dc.contributor.authorThomson, Timothy M
dc.date.accessioned2019-09-25T05:59:19Z
dc.date.available2019-09-25T05:59:19Z
dc.date.issued2008-10
dc.identifier.citationBMC Cancer. 2008; 8:315es_ES
dc.identifier.issn1471-2407es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8377
dc.description.abstractBACKGROUND: 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. 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 co-regulated genes and validation by fluorescent in situ hybridization (FISH). 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. 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.es_ES
dc.description.sponsorshipThis study was supported by grants from the Ministerio de Educación (GEN2001-4856-C13, GEN2001-4865-C13-10 and SAF200505109), 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.es_ES
dc.language.isoenges_ES
dc.publisherBiomed Centrales_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshAdenocarcinoma es_ES
dc.subject.meshCell Line, Tumor es_ES
dc.subject.meshGene Dosage es_ES
dc.subject.meshHumans es_ES
dc.subject.meshImmunohistochemistry es_ES
dc.subject.meshIn Situ Hybridization, Fluorescence es_ES
dc.subject.meshMale es_ES
dc.subject.meshNucleic Acid Hybridization es_ES
dc.subject.meshProstatic Neoplasms es_ES
dc.subject.meshReverse Transcriptase Polymerase Chain Reaction es_ES
dc.subject.meshTranscription, Genetices_ES
dc.subject.meshChromosome Aberrations es_ES
dc.subject.meshChromosomes, Human, Pair 17 es_ES
dc.subject.meshGene Expression Regulation, Neoplastic es_ES
dc.titleCo-regulation analysis of closely linked genes identifies a highly recurrent gain on chromosome 17q25.3 in prostate canceres_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID18973659es_ES
dc.format.volume8es_ES
dc.format.number1es_ES
dc.format.page315es_ES
dc.identifier.doi10.1186/1471-2407-8-315es_ES
dc.contributor.funderMinisterio de Educación (España)es_ES
dc.contributor.funderMinisterio de Sanidad (España)es_ES
dc.contributor.funderFundacio la Maratoes_ES
dc.contributor.funderInstituto de Salud Carlos III - ISCIIIes_ES
dc.contributor.funderFundación Ramón Areceses_ES
dc.identifier.e-issn1471-2407es_ES
dc.relation.publisherversionhttps://doi.org/10.1186/1471-2407-8-315es_ES
dc.identifier.journalBMC canceres_ES
dc.repisalud.orgCNICCNIC::Unidades técnicas::Genómicaes_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución 4.0 Internacional
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