Peinado, PaolaAndrades, AlvaroCuadros, MartaRodriguez, Maria IsabelCoira, Isabel FGarcia, Daniel JBenitez-Cantos, Maria SCano, CarlosZarzuela, EduardoMuñoz, JavierLoidi, ClaudiaSaiz, MonicaMedina, Pedro P2023-05-032023-05-032022-03-17http://hdl.handle.net/10668/20358SWI/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.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/EpigeneticsLung adenocarcinomaLung cancerMulti-omicsPrognosisSWI/SNF complexAdenocarcinoma of LungDNA MethylationDNA-Binding ProteinsHumansLung NeoplasmsTranscription Factorsresearch article35300733open access10.1186/s13148-022-01261-31868-7083PMC8931969https://clinicalepigeneticsjournal.biomedcentral.com/track/pdf/10.1186/s13148-022-01261-3https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8931969/pdf