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dc.contributor.authorPeinado Fernández, Paola 
dc.contributor.authorAndrades Delgado, Álvaro 
dc.contributor.authorCuadros Celorrio, Marta Eugenia 
dc.contributor.authorRodríguez Lara, María Isabel 
dc.contributor.authorGarcía García, Daniel Jesús 
dc.contributor.authorBenítez Cantos, María Soledad 
dc.contributor.authorCano Gutiérrez, Carlos 
dc.contributor.authorMedina Vico, Pedro Pablo
dc.identifier.citationPeinado, P... [et al.]. Multi-omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinoma. Clin Epigenet 14, 42 (2022). []es_ES
dc.descriptionPPM's lab is funded by the Ministry of Economy of Spain (SAF2015-67919-R), Junta de Andalucia (P20-00688, PI-0135-2020, PIGE-0213-2020, PIGE-04402019, PI-0245-2017), University of Granada (B-CTS-480-UGR20), International Association for the Study of Lung Cancer (IASLC), and Spanish Association for Cancer Research (LAB-AECC-2018). PP is supported by a PhD "La Caixa Foundation"LCF/BQ/DE15/10360019 Fellowship. AA is supported by an FPU17/00067 fellowship. IFC was supported by a PhD FPI-fellowship (BES-2013-064596). DJG was supported by a "Fundacion Benefica Anticancer Santa Candida y San Francisco Javier"predoctoral fellowship. MSBC and CC's work is supported by the project DPI2017-84439-R Ministry of Economy of Spain and FEDER and by the fellowship "Beca de Iniciacion a la Investigacion del Plan Propio de Investigacion 2019" by University of Granada. MSBC is supported by an FPU19/00576 predoctoral fellowship. CNIO Proteomics Unit is a member of Proteored PRB3 and is supported by grant PT17/0019, of the PE I + D + i 2013-2016, funded by ISCIII and ERDF.es_ES
dc.description.abstractSWI/SNF complexes are major targets of mutations in cancer. Here, we combined multiple “-omics” methods to assess SWI/SNF composition and aberrations in LUAD. Mutations in lung SWI/SNF subunits were highly recurrent in our LUAD cohort (41.4%), and over 70% of the mutations were predicted to have functional impact. Furthermore, SWI/ SNF expression in LUAD suffered an overall repression that could not be explained exclusively by genetic alterations. Finally, SWI/SNF mutations were associated with poorer overall survival in TCGA-LUAD. We propose SWI/SNF-mutant LUAD as a separate clinical subgroup with practical implications.es_ES
dc.description.sponsorshipSpanish Government SAF2015-67919-R DPI2017-84439-Res_ES
dc.description.sponsorshipJunta de Andalucia P20-00688 PI-0135-2020 PIGE-0213-2020 PIGE-0440-2019 PI-0245-2017es_ES
dc.description.sponsorshipUniversity of Granada B-CTS-480-UGR20es_ES
dc.description.sponsorshipInternational Association for the Study of Lung Cancer (IASLC)es_ES
dc.description.sponsorshipSpanish Association for Cancer Research LAB-AECC-2018es_ES
dc.description.sponsorshipLa Caixa Foundation LCF/BQ/DE15/10360019es_ES
dc.description.sponsorshipPhD FPI-fellowship BES-2013-064596es_ES
dc.description.sponsorship"Fundacion Benefica Anticancer Santa Candida y San Francisco Javier" predoctoral fellowshipes_ES
dc.description.sponsorshipEuropean Commissiones_ES
dc.description.sponsorshipfellowship "Beca de Iniciacion a la Investigacion del Plan Propio de Investigacion 2019" by University of Granada Instituto de Salud Carlos III PT17/0019es_ES
dc.description.sponsorshipEuropean Commission PT17/0019 FPU17/00067 FPU19/00576es_ES
dc.rightsAtribución 3.0 España*
dc.subjectLung canceres_ES
dc.subjectLung adenocarcinomaes_ES
dc.subjectSWI/SNF complexes_ES
dc.subjectPrognosis es_ES
dc.titleMulti‑omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinomaes_ES

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Atribución 3.0 España
Except where otherwise noted, this item's license is described as Atribución 3.0 España