Evidence map›Paper›PMID 19095950›Full record

ArticleThe American journal of pathology2009

Irs2 inactivation suppresses tumor progression in Pten+/- mice.

Matthias Szabolcs, Megan Keniry, Laura Simpson, Latarsha J Reid, Susan Koujak, Sarah C Schiff, Giselle Davidian, Scott Licata, Sofia Gruvberger-Saal, Vundavalli V V S Murty and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. miR-106a* inhibits the proliferation of renal carcinoma cells by targeting IRS-2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. IRS2 is a candidate driver oncogene on 13q34 in colorectal cancer.International journal of experimental pathology · 2013
    Article
  13. Article
  14. Article
  15. Article
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

15 authors at 4 institutions in 1 country.

Matthias SzabolcsInstitute for Cancer Genetics, College of Physicians and Surgeons, Columbia University, New York, New York, USA.
Megan Keniry
Laura Simpson
Latarsha J Reid
Susan Koujak
Sarah C Schiff
Giselle Davidian
Scott Licata
Sofia Gruvberger-Saal
Vundavalli V V S Murty
Subhadra Nandula
Argiris Efstratiadis
Jake A Kushner
Morris F White
Ramon Parsons
Columbia University · USCancer Genetics (United States) · USHarvard University · USPhiladelphia University · US

Funding

PTEN TUMOR SUPPRESSOR AND SIGNAL TRANSDUCTIONR01CA082783 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI PARSONS, RAMON E · 2001 to 2016
$3.8M
PI-3 Kinase Therapy in Mouse Tumor ModelsR01CA099523 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PARSONS, RAMON E · 2002 to 2005
$2.1M
STRUCTURE AND FUNCTION OF THE IRS SIGNALING SYSTEMR01DK043808 · NIDDK · JOSLIN DIABETES CENTER · PI WHITE, MORRIS F. · 1991 to 2004
$1.7M
NCI NIH HHS CA082783NCI NIH HHS CA099523NCI NIH HHS R01 CA082783NCI NIH HHS R01 CA099523NIDDK NIH HHS DK43808NIDDK NIH HHS R01 DK043808
6 · The paper itself

Abstract

Mutations in the phosphatase and tensin homologue (PTEN)/phosphatidylinositol-3 kinase-alpha (PI3K) signaling pathway are frequently found in human cancer. In addition, Pten(+/-) mice develop tumors in multiple organs because of the activation of the PI3K signaling cascade. Because activation of PI3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstream activator of PI3K, we therefore anticipated that IRS2 expression would be low in tumors that lack PTEN. Surprisingly, however, an elevation of IRS2 was often detected in tumor samples in which PTEN levels were compromised. To determine the potential contribution of Irs2 to tumor progression, Pten(+/-) mice were crossed with Irs2(+/-) mice. Deletion of Irs2 did not affect the initiation of neoplasia found in Pten(+/-) mice but suppressed cancer cell growth, proliferation, and invasion through the basement membrane. Deletion of Irs2 also attenuated the expression of Myc in prostatic intraepithelial neoplasia in Pten(+/-) mice. In addition, the expression levels of IRS2 and MYC were highly correlated in human prostate cancer, and IRS2 could stimulate MYC expression in cultured cells. Our findings provide evidence that the PI3K-activating adaptor Irs2 contributes to tumor progression in Pten(+/-) mice by stimulating both Myc and DNA synthesis.

Indexed as

AnimalsBlotting, WesternCell Line, TumorDisease ProgressionEndometrial NeoplasmsFemaleHumansImmunohistochemistryIn Situ HybridizationInsulin Receptor Substrate ProteinsMaleMiceMice, Mutant StrainsNeoplasmsProstatic NeoplasmsProto-Oncogene Proteins c-mycInsulin Receptor Substrate ProteinsIrs2 protein, mouseProto-Oncogene Proteins c-mycPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID19095950
PMCPMC2631340
OpenAlexW2093663627

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.