Evidence map›Paper›PMID 28783178›Full record

ArticleOncogene2017

Fibroblast growth factor receptor is a mechanistic link between visceral adiposity and cancer.

D Chakraborty, V Benham, B Bullard, T Kearney, H C Hsia, D Gibbon, E Y Demireva, S Y Lunt, J J Bernard

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-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

30 citing papers in PubMed, 39 citations in OpenAlex.

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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

9 authors at 4 institutions in 1 country.

D ChakrabortyDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA.
V BenhamDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA.
B BullardDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA.
T KearneyDivision of Surgical Oncology, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA.
H C HsiaSection of Plastic Surgery, Department of Surgery, Yale School of Medicine, New Haven, CT, USA.
D GibbonSummit Medical4 Group, Livingston, NJ, USA.
E Y DemirevaOffice for the Vice President for Research and Graduate Studies, Michigan State University, East Lansing, MI, USA.
S Y LuntDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI, USA.
J J BernardDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, USA.
Michigan State University · USRutgers, The State University of New Jersey · USSummit Medical Group (United States) · USYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
The Role of Fat in Tumor FormationR00CA177868 · NCI · MICHIGAN STATE UNIVERSITY · PI BERNARD, JAMIE J · 2015 to 2017
$699k
The Role of Fat in Tumor FormationK99CA177868 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI BERNARD, JAMIE J · 2014 to 2014
$89k
NCATS NIH HHS UL1 TR001863NCI NIH HHS K99 CA177868NCI NIH HHS R00 CA177868
6 · The paper itself

Abstract

Epidemiological evidence implicates excess adipose tissue in increasing cancer risk. Despite a steeply rising global prevalence of obesity, how adiposity contributes to transformation (stage a non-tumorigenic cell undergoes to become malignant) is unknown. To determine the factors in adipose tissue that stimulate transformation, we used a novel ex vivo system of visceral adipose tissue (VAT)-condition medium-stimulated epithelial cell growth in soft agar. To extend this system in vivo, we used a murine lipectomy model of ultraviolet light B-induced, VAT-promoted skin tumor formation. We found that VAT from mice and obese human donors stimulated growth in soft agar of non-tumorigenic epithelial cells. The difference in VAT activity was associated with fibroblast growth factor-2 (FGF2) levels. Moreover, human and mouse VAT failed to stimulate growth in soft of agar in cells deficient in FGFR-1 (FGF2 receptor). We also demonstrated that circulating levels of FGF2 were associated with non-melanoma tumor formation in vivo. These data implicate FGF2 as a major factor VAT releases to transform epithelial cells-a novel, potential pathway of VAT-enhanced tumorigenesis. Strategies designed to deplete VAT stores of FGF2 or inhibit FGFR-1 in abdominally obese individuals may be important cancer prevention strategies as well as adjuvant therapies for improving outcomes.

Indexed as

AnimalsCell LineCell Transformation, NeoplasticDiet, High-FatFemaleFibroblast Growth Factor 2HumansIntra-Abdominal FatMice, Inbred StrainsReceptor, Fibroblast Growth Factor, Type 1Signal TransductionFgfr1 protein, mouseFibroblast Growth Factor 2Receptor, Fibroblast Growth Factor, Type 1

Identifiers

PMID28783178
PMCPMC5709202
OpenAlexW2743188042

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.