Journal
CLINICAL EPIGENETICS
Volume 14, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s13148-022-01261-3
Keywords
Multi-omics; Lung cancer; Lung adenocarcinoma; SWI; SNF complex; Epigenetics; Prognosis
Categories
Funding
- Ministry of Economy of Spain [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
- FEDER
- fellowship Beca de Iniciacion a la Investigacion del Plan Propio de Investigacion 2019 by University of Granada
- ISCIII [PT17/0019]
- ERDF [PT17/0019]
- [FPU17/00067]
- [FPU19/00576]
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We used multiple -omics methods to assess SWI/SNF composition and aberrations in LUAD. Mutations in lung SWI/SNF subunits were highly recurrent and predicted to have functional impact. SWI/SNF expression in LUAD suffered overall repression and mutations were associated with poorer overall survival.
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.
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