Evidence map›Paper›PMID 17486056›Full record

ArticleOncogene2007

Loss of PTEN selectively desensitizes upstream IGF1 and insulin signaling.

J Lackey, J Barnett, L Davidson, I H Batty, N R Leslie, C P Downes

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. PTEN is a protein tyrosine phosphatase for IRS1.Nature structural & molecular biology · 2014
    Article
  5. Article
  6. Article
  7. PTEN in liver diseases and cancer.World journal of gastroenterology · 2010
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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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

6 authors at 1 institution in 1 country.

J LackeyDivision of Molecular Physiology, School of Life Sciences, University of Dundee, Dundee, Scotland, UK.
J Barnett
L Davidson
I H Batty
N R Leslie
C P Downes
University of Dundee · GB

Funding

Medical Research Council G9403619Medical Research Council G9403619(67505)
6 · The paper itself

Abstract

Many tumors have chronically elevated activity of PI 3-kinase-dependent signaling pathways, caused largely by oncogenic mutation of PI 3-kinase itself or loss of the opposing tumor suppressor lipid phosphatase, PTEN. Several PI 3-kinase-dependent feedback mechanisms have been identified that may affect the sensitivity of upstream receptor signaling, but the events required to initiate an inhibited state have not been addressed. We show that in a variety of cell types, loss of PTEN via experimental knockdown or in tumor cell lines correlates with a block in insulin-like growth factor 1 (IGF1)/insulin signaling, without affecting the sensitivity of platelet-derived growth factor or epidermal growth factor signaling. These effects on IGF/insulin signaling include a reduction of up to five- to tenfold in IGF-stimulated PI 3-kinase activation, a failure to activate the ERK kinases and, in some cells, reduced expression of insulin receptor substrate 1, and both IGF1 and insulin receptors. These data indicate that chronically elevated PI 3-kinase-dependent signaling to the degree seen in many tumors causes a selective loss of sensitivity in IGF1/insulin signaling that could significantly reduce the selective advantage of deregulated activation of IGF1/IGF1-R signaling in tumor development.

Indexed as

AnimalsCell LineCell Line, TumorDogsHumansInsulinInsulin-Like Growth Factor IMiceNIH 3T3 CellsPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPTEN PhosphohydrolaseSignal TransductionInsulinInsulin-Like Growth Factor Iphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID17486056
PMCPMC2773499
OpenAlexW2026452577

What OpenQuestion holds

Textmetadata
LicenceTDM
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.