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dc.contributor.authorIbáñez, Kristina
dc.contributor.authorBoullosa, César
dc.contributor.authorTabarés-Seisdedos, Rafael
dc.contributor.authorBaudot, Anaïs
dc.contributor.authorValencia, Alfonso 
dc.date.accessioned2020-11-25T10:19:29Z
dc.date.available2020-11-25T10:19:29Z
dc.date.issued2014-02
dc.identifier.citationPLoS Genet .2014;10(2):e1004173.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/11419
dc.description.abstractThere is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.es_ES
dc.description.sponsorshipThis work was supported by a Fellowship from Obra Social la Caixa grant to KI (http://obrasocial.lacaixa.es/laCaixaFoundation/home_en.html), FPI grant BES-2008-006332 to CB and grant BIO2012 to AV Group. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.es_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Science (PLOS) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshComorbidity es_ES
dc.subject.meshAlzheimer Disease es_ES
dc.subject.meshCentral Nervous System es_ES
dc.subject.meshGene Expression Profiling es_ES
dc.subject.meshGene Expression Regulation es_ES
dc.subject.meshHumans es_ES
dc.subject.meshNIMA-Interacting Peptidylprolyl Isomerase es_ES
dc.subject.meshNeoplasms es_ES
dc.subject.meshParkinson Disease es_ES
dc.subject.meshPeptidylprolyl Isomerase es_ES
dc.subject.meshSchizophrenia es_ES
dc.subject.meshSignal Transduction es_ES
dc.titleMolecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID24586201es_ES
dc.format.volume10es_ES
dc.format.number2es_ES
dc.format.pagee1004173es_ES
dc.identifier.doi10.1371/journal.pgen.1004173es_ES
dc.contributor.funderFundación La Caixa 
dc.contributor.funderMinisterio de Economía y Competitividad (España) 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1371/journal.pgen.1004173es_ES
dc.identifier.journalPLoS geneticses_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Antiguos CNIOes_ES
dc.relation.projectIDinfo:eu_repo/grantAgreement/ES/BES-2008-006332es_ES
dc.rights.accessRightsopen accesses_ES


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