Multi‑omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinoma
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AuthorPeinado Fernández, Paola; Andrades Delgado, Álvaro; Cuadros Celorrio, Marta Eugenia; Rodríguez Lara, María Isabel; García García, Daniel Jesús; Benítez Cantos, María Soledad; Cano Gutiérrez, Carlos; Medina Vico, Pedro Pablo
Multi-omicsLung cancerLung adenocarcinomaSWI/SNF complexEpigeneticsPrognosis
Peinado, P... [et al.]. Multi-omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinoma. Clin Epigenet 14, 42 (2022). [https://doi.org/10.1186/s13148-022-01261-3]
SponsorshipSpanish Government SAF2015-67919-R DPI2017-84439-R; Junta de Andalucia P20-00688 PI-0135-2020 PIGE-0213-2020 PIGE-0440-2019 PI-0245-2017; University of Granada B-CTS-480-UGR20; International Association for the Study of Lung Cancer (IASLC); Spanish Association for Cancer Research LAB-AECC-2018; La Caixa Foundation LCF/BQ/DE15/10360019; PhD FPI-fellowship BES-2013-064596; "Fundacion Benefica Anticancer Santa Candida y San Francisco Javier" predoctoral fellowship; European Commission; fellowship "Beca de Iniciacion a la Investigacion del Plan Propio de Investigacion 2019" by University of Granada Instituto de Salud Carlos III PT17/0019; European Commission PT17/0019 FPU17/00067 FPU19/00576
SWI/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.