Evidence map›Paper›PMID 21892209›Full record

ArticleOncogene2012

An integrated genomic approach identifies ARID1A as a candidate tumor-suppressor gene in breast cancer.

A Mamo, L Cavallone, S Tuzmen, C Chabot, C Ferrario, S Hassan, H Edgren, O Kallioniemi, O Aleynikova, E Przybytkowski and 4 more

Abstract read
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In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Molecular medicine reports · 2024
    Article
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  7. Therapeutic Role of Synthetic Lethality inJournal of immunotherapy and precision oncology · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. ARID1A in cancer: Friend or foe?Frontiers in oncology · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 3 countries.

A MamoDepartment of Oncology, Lady Davis Institute, Sir Mortimer B Davis Jewish General Hospital, McGill University, Montreal, Québec, Canada.
L Cavallone
S Tuzmen
C Chabot
C Ferrario
S Hassan
H Edgren
O Kallioniemi
O Aleynikova
E Przybytkowski
K Malcolm
S Mousses
P N Tonin
M Basik
Jewish General Hospital · CAMcGill University · CATranslational Genomics Research Institute · USInstitute for Molecular Medicine Finland · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-suppressor genes (TSGs) have been classically defined as genes whose loss of function in tumor cells contributes to the formation and/or maintenance of the tumor phenotype. TSGs containing nonsense mutations may not be expressed because of nonsense-mediated RNA decay (NMD). We combined inhibition of the NMD process, which clears transcripts that contain nonsense mutations, with the application of high-density single-nucleotide polymorphism arrays analysis to discriminate allelic content in order to identify candidate TSGs in five breast cancer cell lines. We identified ARID1A as a target of NMD in the T47D breast cancer cell line, likely as a consequence of a mutation in exon-9, which introduces a premature stop codon at position Q944. ARID1A encodes a human homolog of yeast SWI1, which is an integral member of the hSWI/SNF complex, an ATP-dependent, chromatin-remodeling, multiple-subunit enzyme. Although we did not find any somatic mutations in 11 breast tumors, which show DNA copy-number loss at the 1p36 locus adjacent to ARID1A, we show that low ARID1A RNA or nuclear protein expression is associated with more aggressive breast cancer phenotypes, such as high tumor grade, in two independent cohorts of over 200 human breast cancer cases each. We also found that low ARID1A nuclear expression becomes more prevalent during the later stages of breast tumor progression. Finally, we found that ARID1A re-expression in the T47D cell line results in significant inhibition of colony formation in soft agar. These results suggest that ARID1A may be a candidate TSG in breast cancer.

Indexed as

Genes, Tumor SuppressorBreast NeoplasmsCell Line, TumorChromosomes, Human, Pair 1Codon, NonsenseDNA-Binding ProteinsDNA Copy Number VariationsFemaleHumansNuclear ProteinsRNATranscription FactorsTransfectionARID1A protein, humanCodon, NonsenseDNA-Binding ProteinsNuclear ProteinsRNATranscription Factors

Identifiers

PMID21892209
OpenAlexW1968702293

What OpenQuestion holds

Textmetadata
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.