Evidence map›Paper›PMID 23594372›Full record

ArticleInternational journal of experimental pathology2013

IRS2 is a candidate driver oncogene on 13q34 in colorectal cancer.

Elizabeth Day, George Poulogiannis, Frank McCaughan, Shani Mulholland, Mark J Arends, Ashraf E K Ibrahim, Paul H Dear

Open access · bronzeAbstract read
In one paragraph

Article in International journal of experimental pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Deciphering of SOX9 Functions in Pancreatic Cancer Cells.International journal of molecular sciences · 2025
    Article
  8. Integrative Computational Framework,bioRxiv : the preprint server for biology · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Molecular therapy oncolytics · 2020
    Article
  18. Review
  19. Article
  20. Etiology of Metabolic Syndrome and Dietary Intervention.International journal of molecular sciences · 2018
    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

7 authors at 3 institutions in 2 countries.

Elizabeth DayMRC Laboratory of Molecular Biology, Cambridge, UK.
George Poulogiannis
Frank McCaughan
Shani Mulholland
Mark J Arends
Ashraf E K Ibrahim
Paul H Dear
MRC Laboratory of Molecular Biology · GBUniversity of Cambridge · GBBeth Israel Deaconess Medical Center · US

Funding

Cancer Research UK 11388Cancer Research UK WT097143MAMedical Research Council G0500392Medical Research Council MC_U105131672Wellcome Trust
6 · The paper itself

Abstract

Copy number alterations are frequently found in colorectal cancer (CRC), and recurrent gains or losses are likely to correspond to regions harbouring genes that promote or impede carcinogenesis respectively. Gain of chromosome 13q is common in CRC but, because the region of gain is frequently large, identification of the driver gene(s) has hitherto proved difficult. We used array comparative genomic hybridization to analyse 124 primary CRCs, demonstrating that 13q34 is a region of gain in 35% of CRCs, with focal gains in 4% and amplification in a further 1.6% of cases. To reduce the number of potential driver genes to consider, it was necessary to refine the boundaries of the narrowest copy number changes seen in this series and hence define the minimal copy region (MCR). This was performed using molecular copy-number counting, identifying IRS2 as the only complete gene, and therefore the likely driver oncogene, within the refined MCR. Analysis of available colorectal neoplasia data sets confirmed IRS2 gene gain as a common event. Furthermore, IRS2 protein and mRNA expression in colorectal neoplasia was assessed and was positively correlated with progression from normal through adenoma to carcinoma. In functional in vitro experiments, we demonstrate that deregulated expression of IRS2 activates the oncogenic PI3 kinase pathway and increases cell adhesion, both characteristics of invasive CRC cells. Together, these data identify IRS2 as a likely driver oncogene in the prevalent 13q34 region of gain/amplification and suggest that IRS2 over-expression may provide an additional mechanism of PI3 kinase pathway activation in CRC.

Indexed as

Chromosomes, Human, Pair 13AdenocarcinomaColonic PolypsColorectal NeoplasmsDatabases, GeneticGene DosageGene Expression ProfilingGene Expression Regulation, NeoplasticGenomic InstabilityHumansInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerSignal TransductionAKT1 protein, humanInsulin-Like Growth Factor IInsulin Receptor Substrate ProteinsIRS2 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID23594372
PMCPMC3664965
OpenAlexW2099788018

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.