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dc.contributor.authorForés-Martos, Jaume
dc.contributor.authorCatala-Lopez, Ferran 
dc.contributor.authorSánchez-Valle, Jon
dc.contributor.authorIbáñez, Kristina
dc.contributor.authorTejero Franco, Hector 
dc.contributor.authorPalma-Gudiel, Helena
dc.contributor.authorCliment, Joan
dc.contributor.authorPancaldi, Vera
dc.contributor.authorFañanás, Lourdes
dc.contributor.authorArango, Celso
dc.contributor.authorParellada, Mara
dc.contributor.authorBaudot, Anaïs
dc.contributor.authorVogt, Daniel
dc.contributor.authorRubenstein, John L
dc.contributor.authorValencia, Alfonso 
dc.contributor.authorTabarés-Seisdedos, Rafael
dc.date.accessioned2019-05-21T08:14:35Z
dc.date.available2019-05-21T08:14:35Z
dc.date.issued2019
dc.identifier.citationMol Autism. 2019 ;10:17.es_ES
dc.identifier.issn2040-2392es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/7618
dc.description.abstractBackground: Epidemiological and clinical evidence points to cancer as a comorbidity in people with autism spectrum disorders (ASD). A significant overlap of genes and biological processes between both diseases has also been reported. Methods: Here, for the first time, we compared the gene expression profiles of ASD frontal cortex tissues and 22 cancer types obtained by differential expression meta-analysis and report gene, pathway, and drug set-based overlaps between them. Results: Four cancer types (brain, thyroid, kidney, and pancreatic cancers) presented a significant overlap in gene expression deregulations in the same direction as ASD whereas two cancer types (lung and prostate cancers) showed differential expression profiles significantly deregulated in the opposite direction from ASD. Functional enrichment and LINCS L1000 based drug set enrichment analyses revealed the implication of several biological processes and pathways that were affected jointly in both diseases, including impairments of the immune system, and impairments in oxidative phosphorylation and ATP synthesis among others. Our data also suggest that brain and kidney cancer have patterns of transcriptomic dysregulation in the PI3K/AKT/MTOR axis that are similar to those found in ASD. Conclusions: Comparisons of ASD and cancer differential gene expression meta-analysis results suggest that brain, kidney, thyroid, and pancreatic cancers are candidates for direct comorbid associations with ASD. On the other hand, lung and prostate cancers are candidates for inverse comorbid associations with ASD. Joint perturbations in a set of specific biological processes underlie these associations which include several pathways previously implicated in both cancer and ASD encompassing immune system alterations, impairments of energy metabolism, cell cycle, and signaling through PI3K and G protein-coupled receptors among others. These findings could help to explain epidemiological observations pointing towards direct and inverse comorbid associations between ASD and specific cancer types and depict a complex scenario regarding the molecular patterns of association between ASD and cancer.es_ES
dc.description.sponsorshipProfessor Rafael Tabarés-Seisdedos and Jaume Forés were supported in part by grant number PROMETEOII/2015/021 from Generalitat Valenciana and the national grant PI17/00719 from ISCIII-FEDER.es_ES
dc.language.isoenges_ES
dc.publisherBioMed Central (BMC) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectASDes_ES
dc.subjectAutismes_ES
dc.subjectCanceres_ES
dc.subjectComorbidityes_ES
dc.subjectGene expressiones_ES
dc.subjectMeta-analysises_ES
dc.subjectMultimorbidityes_ES
dc.subjectTranscriptomees_ES
dc.subject.meshAutistic Disorder es_ES
dc.subject.meshBrain es_ES
dc.subject.meshHumans es_ES
dc.subject.meshNeoplasms es_ES
dc.subject.meshSignal Transduction es_ES
dc.subject.meshTranscriptome es_ES
dc.titleTranscriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with canceres_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID31007884es_ES
dc.format.volume10es_ES
dc.format.number1es_ES
dc.format.page17es_ES
dc.identifier.doi10.1186/s13229-019-0262-8es_ES
dc.contributor.funderGeneralitat Valenciana (España) 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn2040-2392es_ES
dc.relation.publisherversionhttps://doi.org/10.1186/s13229-019-0262-8.es_ES
dc.identifier.journalMolecular autismes_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Unidades técnicas::Unidad de Bioinformáticaes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI17/00719es_ES
dc.rights.accessRightsopen accesses_ES


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