Evidence map›Paper›PMID 23650517›Full record

ArticlePloS one2013

ARID1A alterations are associated with FGFR3-wild type, poor-prognosis, urothelial bladder tumors.

Cristina Balbás-Martínez, María Rodríguez-Pinilla, Ariel Casanova, Orlando Domínguez, David G Pisano, Gonzalo Gómez, Josep Lloreta, José A Lorente, Núria Malats, Francisco X Real

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. The Role of SWI/SNF Complex in Bladder Cancer.Journal of cellular and molecular medicine · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Role of ARID1A in the Regulation of Human Trophoblast Migration and Invasion.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Article
  10. Article
  11. SWI/SNF chromatin remodeling complex alterations in meningioma.Journal of cancer research and clinical oncology · 2021
    Article
  12. Targeted Deep Sequencing of Bladder Tumors Reveals Novel Associations between Cancer Gene Mutations and Mutational Signatures with Major Risk Factors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Epigenetic Alterations in Bladder Cancer.Current urology reports · 2018
    Review
  18. Review
  19. Unmasking molecular profiles of bladder cancer.Investigative and clinical urology · 2018
    Review
  20. The diagnostic role of PTEN and ARID1A in serous effusions.Virchows Archiv : an international journal of pathology · 2018
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Cristina Balbás-MartínezEpithelial Carcinogenesis Group, Molecular Pathology Programme, Spanish National Cancer Research Centre, Madrid, Spain.
María Rodríguez-Pinilla
Ariel Casanova
Orlando Domínguez
David G Pisano
Gonzalo Gómez
Josep Lloreta
José A Lorente
Núria Malats
Francisco X Real
Spanish National Cancer Research Centre · ESHospital Del Mar · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urothelial bladder cancer (UBC) is heterogeneous at the clinical, pathological, genetic, and epigenetic levels. Exome sequencing has identified ARID1A as a novel tumor suppressor gene coding for a chromatin remodeling protein that is mutated in UBC. Here, we assess ARID1A alterations in two series of patients with UBC. In the first tumor series, we analyze exons 2-20 in 52 primary UBC and find that all mutant tumors belong to the aggressive UBC phenotype (high grade non-muscle invasive and muscle invasive tumors) (P = 0.05). In a second series (n = 84), we assess ARID1A expression using immunohistochemistry, a surrogate for mutation analysis, and find that loss of expression increases with higher stage/grade, it is inversely associated with FGFR3 overexpression (P = 0.03) but it is not correlated with p53 overexpression (P = 0.30). We also analyzed the expression of cytokeratins in the same set of tumor and find, using unsupervised clustering, that tumors with ARID1A loss of expression are generally KRT5/6-low. In this patient series, loss of ARID1A expression is also associated with worse prognosis, likely reflecting the higher prevalence of losses found in tumors of higher stage and grade. The independent findings in these two sets of patients strongly support the notion that ARID1A inactivation is a key player in bladder carcinogenesis occurring predominantly in FGFR3 wild type tumors.

Indexed as

AgedAged, 80 and overBase SequenceCarcinoma, Transitional CellCell Line, TumorDNA-Binding ProteinsDNA Mutational AnalysisFemaleHEK293 CellsHumansKaplan-Meier EstimateMaleMiddle AgedMutation, MissenseNuclear ProteinsPrognosisARID1A protein, humanDNA-Binding ProteinsFGFR3 protein, humanNuclear ProteinsReceptor, Fibroblast Growth Factor, Type 3TP53 protein, humanTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID23650517
PMCPMC3641081
OpenAlexW1983641328

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.