Evidence map›Paper›PMID 35300733›Full record

ArticleClinical epigenetics2022

Multi-omic alterations of the SWI/SNF complex define a clinical subgroup in lung adenocarcinoma.

Paola Peinado, Alvaro Andrades, Marta Cuadros, Maria Isabel Rodriguez, Isabel F Coira, Daniel J Garcia, Maria S Benitez-Cantos, Carlos Cano, Eduardo Zarzuela, Javier Muñoz and 3 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Paola Peinado *Department of Biochemistry and Molecular Biology I, University of Granada, Campus Fuentenueva s/n, 18071, Granada, Spain.
Alvaro Andrades *Department of Biochemistry and Molecular Biology I, University of Granada, Campus Fuentenueva s/n, 18071, Granada, Spain.
Marta Cuadros *GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain.
Maria Isabel Rodriguez *GENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain.
Isabel F CoiraSchool of Pharmaceutical Sciences, University of Geneva, Geneva, Switzerland.
Daniel J GarciaGENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain.
Maria S Benitez-CantosGENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, Granada, Spain.
Carlos CanoDepartment of Computer Science and Artificial Intelligence, University of Granada, Granada, Spain.
Eduardo ZarzuelaProteomics Unit, Spanish National Cancer Research Center, CNIO. Proteored-ISCIII, Madrid, Spain.
Javier MuñozProteomics Unit, Spanish National Cancer Research Center, CNIO. Proteored-ISCIII, Madrid, Spain.
Claudia LoidiPathological Anatomy, Universitary Hospital Cruces, University of Pais Vasco, Gipuzkoa, Spain.
Monica SaizPathological Anatomy, Universitary Hospital Cruces, University of Pais Vasco, Gipuzkoa, Spain.
Pedro P MedinaDepartment of Biochemistry and Molecular Biology I, University of Granada, Campus Fuentenueva s/n, 18071, Granada, Spain. pedromedina@ugr.es.ORCID 0000-0002-7834-7093
Universidad de Granada · ESHospital de Cruces · ESSpanish National Cancer Research Centre · ESUniversity of Geneva · CH

Funding

Fundación Científica Asociación Española Contra el Cáncer LAB-AECC-2018Junta de Andalucía P20-00688Junta de Andalucía PI-0135-2020Junta de Andalucía PI-0245-2017Junta de Andalucía PIGE-0213-2020Junta de Andalucía PIGE-0440-2019Ministerio de Economía y Competitividad DPI2017-84439-RMinisterio de Economía y Competitividad SAF2015-67919-RUniversidad de Granada B-CTS-480-UGR20
6 · The paper itself

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.

Indexed as

Adenocarcinoma of LungLung NeoplasmsDNA-Binding ProteinsDNA MethylationHumansTranscription FactorsDNA-Binding ProteinsTranscription FactorsEpigeneticsLung adenocarcinomaLung cancerMulti-omicsPrognosisSWI/SNF complex

Identifiers

PMID35300733
PMCPMC8931969
OpenAlexW4221124880

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.