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dc.contributor.authorLupiañez, Carmen B
dc.contributor.authorVillaescusa, María T
dc.contributor.authorCarvalho, Agostinho
dc.contributor.authorSpringer, Jan
dc.contributor.authorLackner, Michaela
dc.contributor.authorSánchez-Maldonado, Jose Manuel
dc.contributor.authorCanet, Luz M
dc.contributor.authorCunha, Cristina
dc.contributor.authorSegura-Catena, Juana
dc.contributor.authorAlcazar-Fuoli, Laura 
dc.contributor.authorSolano, Carlos
dc.contributor.authorFianchi, Luana
dc.contributor.authorPagano, Livio
dc.contributor.authorPotenza, Leonardo
dc.contributor.authorAguado, José María
dc.contributor.authorLuppi, Mario
dc.contributor.authorCuenca-Estrella, Manuel 
dc.contributor.authorLass-Flörl, Cornelia
dc.contributor.authorEinsele, Hermann
dc.contributor.authorVázquez, Lourdes
dc.contributor.authorRíos-Tamayo, Rafael
dc.contributor.authorLoeffler, Jurgen
dc.contributor.authorJurado, Manuel
dc.contributor.authorSainz, Juan
dc.date.accessioned2020-02-21T10:57:15Z
dc.date.available2020-02-21T10:57:15Z
dc.date.issued2016
dc.identifier.citationFront Microbiol. 2016 Aug 12;7:1243.es_ES
dc.identifier.issn1664-302Xes_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9127
dc.description.abstractInvasive Aspergillosis (IA) is an opportunistic infection caused by Aspergillus, a ubiquitously present airborne pathogenic mold. A growing number of studies suggest a major host genetic component in disease susceptibility. Here, we evaluated whether 14 single-nucleotide polymorphisms within NFκB1, NFκB2, RelA, RelB, Rel, and IRF4 genes influence the risk of IA in a population of 834 high-risk patients (157 IA and 677 non-IA) recruited through a collaborative effort involving the aspBIOmics consortium and four European clinical institutions. No significant overall associations between selected SNPs and the risk of IA were found in this large cohort. Although a hematopoietic stem cell transplantation (HSCT)-stratified analysis revealed that carriers of the IRF4 rs12203592T/T genotype had a six-fold increased risk of developing the infection when compared with those carrying the C allele (ORREC = 6.24, 95%CI 1.25-31.2, P = 0.026), the association of this variant with IA risk did not reach significance at experiment-wide significant threshold. In addition, we found an association of the IRF4AATC and IRF4GGTC haplotypes (not including the IRF4 rs12203592T risk allele) with a decreased risk of IA but the magnitude of the association was similar to the one observed in the single-SNP analysis, which indicated that the haplotypic effect on IA risk was likely due to the IRF4 rs12203592 SNP. Finally, no evidence of significant interactions among the genetic markers tested and the risk of IA was found. These results suggest that the SNPs on the studied genes do not have a clinically relevant impact on the risk of developing IA.es_ES
dc.description.sponsorshipThis study was supported by grants PI12/02688 from Fondo de Investigaciones Sanitarias (Instituto de Salud Carlos III, Madrid, Spain), the ERA-NET PathoGenoMics (03159000A; Ministerio de Ciencia e Innovación PIM2010EPA-00756, Madrid, Spain), the Collaborative Research Center / Transregio 124 FungiNet, the Austrian Science Fundation (FWF I-656-B09), the Fundação para a Ciência e Tecnologia (FCT), cofunded by Programa Operacional Regional do Norte (ON.2—O Novo Norte), the Quadro de Referência Estratégico Nacional (QREN) through the Fundo Europeu de Desenvolvimento Regional (FEDER) and the Projeto Estratégico – LA 26 – 2013–2014 (PEst-C/SAU/LA0026/2013). Agostinho Carvalho and Cristina Cunha were supported by the Fundação para a Ciência e Tecnologia (FCT), Portugal (IF/00735/2014 and SFRH/BPD/96176/2013, respectively). The PCRAGA trial was supported by an unrestricted grant from Pfizer, which had no involvement or control over the collection, analysis, and interpretation of data; the writing of the report; or the decision to submit the paper for publication. This study was also supported by Astellas Pharma Inc. and a donation from Consuelo González Moreno, an acute myeloid leukemia survivor.es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Media es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectInvasive Aspergillosises_ES
dc.subjectNFκB-related geneses_ES
dc.subjectgenetic polymorphismses_ES
dc.subjectinteractiones_ES
dc.subjectsusceptibilityes_ES
dc.titleCommon Genetic Polymorphisms within NFκB-Related Genes and the Risk of Developing Invasive Aspergillosises_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID27570521es_ES
dc.format.volume7es_ES
dc.format.page1243es_ES
dc.identifier.doi10.3389/fmicb.2016.01243es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderMinisterio de Ciencia e Innovación (España) 
dc.contributor.funderFWF Austrian Science Fund 
dc.contributor.funderFundação para a Ciência e Tecnologia (Portugal) 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3389/fmicb.2016.01243es_ES
dc.identifier.journalFrontiers in microbiologyes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI12/02688es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/03159000Aes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PIM2010EPA-00756es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/FWF I-656-B09es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PEst-C/SAU/LA0026/2013es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/IF/00735/2014es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SFRH/BPD/96176/2013es_ES
dc.rights.accessRightsopen accesses_ES


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