Evidence map›Paper›PMID 22896210›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2012

Energy balance modulates mouse skin tumor promotion through altered IGF-1R and EGFR crosstalk.

Tricia Moore, Linda Beltran, Steve Carbajal, Stephen D Hursting, John DiGiovanni

Abstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  17. Metformin inhibits skin tumor promotion in overweight and obese mice.Cancer prevention research (Philadelphia, Pa.) · 2014
    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

5 authors at 1 institution in 1 country.

Tricia MooreDivision of Pharmacology and Toxicololgy, College of Pharmacy, The University of Texas at Austin, Austin, Texas 78723, USA.
Linda Beltran
Steve Carbajal
Stephen D Hursting
John DiGiovanni
The University of Texas at Austin · US

Funding

Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
Training in Molecular Toxicology/Environmental DiseaseT32ES007247 · NIEHS · UNIVERSITY OF TEXAS AUSTIN · PI RICHBURG, JOHN H · 1990 to 2014
$2.9M
Akt/mTOR Signaling in Energy Balance Modulation of Epithelial CarcinogenesisR01CA129409 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI HURSTING, STEPHEN D · 2009 to 2013
$1.6M
NCI NIH HHS CA129409NCI NIH HHS R01 CA129409NIEHS NIH HHS ES007247NIEHS NIH HHS P30 ES007784NIEHS NIH HHS P30ES007784NIEHS NIH HHS T32 ES007247
6 · The paper itself

Abstract

Obesity, an established risk factor for epithelial cancers, remains prevalent in the United States and many other countries. In contrast to positive energy balance states (overweight, obesity), calorie restriction (CR) has been shown to act as a universal inhibitor of tumorigenesis in multiple animal models of human cancer. Unfortunately, the mechanisms underlying the enhancing effects of obesity or the inhibitory effects of CR on cancer etiology remain elusive. Here, we evaluated the impact of dietary energy balance manipulation on epithelial carcinogenesis and identified several potential mechanisms that may account for the differential effects of obesity and CR on cancer. Obesity enhanced tumor promotion during epithelial carcinogenesis, in part, due to altered insulin-like growth factor-1 receptor (IGF-1R)/EGF receptor (EGFR) crosstalk and downstream signaling to effectors such as Akt/mTOR. Obesity-induced changes in cellular signaling subsequently led to altered levels of cell-cycle proteins that favored enhanced epidermal proliferation during tumor promotion. In contrast, CR reduced susceptibility to tumor promotion, attenuated IGF-1R/EGFR crosstalk and downstream signaling, and altered levels of cell-cycle proteins that favored reduced epidermal proliferation during tumor promotion. Collectively, these findings suggest potential targets for the prevention of epithelial cancers, as well as for reversal of obesity-mediated cancer development and progression. Cancer Prev Res; 5(10); 1236-46. ©2012 AACR.

Indexed as

Energy Metabolism9,10-Dimethyl-1,2-benzanthraceneAnimalsBlotting, WesternCaloric RestrictionCarcinogensCell CycleCell ProliferationCells, CulturedCell Transformation, NeoplasticDietErbB ReceptorsFemaleInsulin-Like Growth Factor IKeratinocytesMice9,10-Dimethyl-1,2-benzanthraceneCarcinogensEGFR protein, mouseErbB ReceptorsInsulin-Like Growth Factor ImTOR protein, mouseProto-Oncogene Proteins c-aktReceptor, IGF Type 1RNA, MessengerTOR Serine-Threonine Kinases

Identifiers

PMID22896210
PMCPMC3482456
OpenAlexW2104938444

What OpenQuestion holds

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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.