Publication: Multi-omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinoma.
dc.contributor.author | Peinado, Paola | |
dc.contributor.author | Andrades, Alvaro | |
dc.contributor.author | Cuadros, Marta | |
dc.contributor.author | Rodriguez, Maria Isabel | |
dc.contributor.author | Coira, Isabel F | |
dc.contributor.author | Garcia, Daniel J | |
dc.contributor.author | Benitez-Cantos, Maria S | |
dc.contributor.author | Cano, Carlos | |
dc.contributor.author | Zarzuela, Eduardo | |
dc.contributor.author | Muñoz, Javier | |
dc.contributor.author | Loidi, Claudia | |
dc.contributor.author | Saiz, Monica | |
dc.contributor.author | Medina, Pedro P | |
dc.date.accessioned | 2023-05-03T13:34:59Z | |
dc.date.available | 2023-05-03T13:34:59Z | |
dc.date.issued | 2022-03-17 | |
dc.description.abstract | 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. | |
dc.identifier.doi | 10.1186/s13148-022-01261-3 | |
dc.identifier.essn | 1868-7083 | |
dc.identifier.pmc | PMC8931969 | |
dc.identifier.pmid | 35300733 | |
dc.identifier.pubmedURL | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8931969/pdf | |
dc.identifier.unpaywallURL | https://clinicalepigeneticsjournal.biomedcentral.com/track/pdf/10.1186/s13148-022-01261-3 | |
dc.identifier.uri | http://hdl.handle.net/10668/20358 | |
dc.issue.number | 1 | |
dc.journal.title | Clinical epigenetics | |
dc.journal.titleabbreviation | Clin Epigenetics | |
dc.language.iso | en | |
dc.organization | Centro Pfizer-Universidad de Granada-Junta de Andalucía de Genómica e Investigación Oncológica-GENYO | |
dc.organization | Instituto de Investigación Biosanitaria de Granada (ibs.GRANADA) | |
dc.page.number | 42 | |
dc.pubmedtype | Journal Article | |
dc.pubmedtype | Research Support, Non-U.S. Gov't | |
dc.rights | Attribution 4.0 International | |
dc.rights.accessRights | open access | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.subject | Epigenetics | |
dc.subject | Lung adenocarcinoma | |
dc.subject | Lung cancer | |
dc.subject | Multi-omics | |
dc.subject | Prognosis | |
dc.subject | SWI/SNF complex | |
dc.subject.mesh | Adenocarcinoma of Lung | |
dc.subject.mesh | DNA Methylation | |
dc.subject.mesh | DNA-Binding Proteins | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Lung Neoplasms | |
dc.subject.mesh | Transcription Factors | |
dc.title | Multi-omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinoma. | |
dc.type | research article | |
dc.type.hasVersion | VoR | |
dc.volume.number | 14 | |
dspace.entity.type | Publication |
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