Evidence map›Paper›PMID 24832086›Full record

ArticleCarcinogenesis2014

Maternal metabolic perturbations elicited by high-fat diet promote Wnt-1-induced mammary tumor risk in adult female offspring via long-term effects on mammary and systemic phenotypes.

Maria Theresa E Montales, Stepan B Melnyk, Frank A Simmen, Rosalia C M Simmen

Open access · greenAbstract read
In one paragraph

Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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  12. Effects of obesity on hormonally driven cancer in women.Science translational medicine · 2016
    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

4 authors at 1 institution in 1 country.

Maria Theresa E MontalesDepartment of Physiology & Biophysics, Department of Pediatrics and Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Stepan B MelnykDepartment of Pediatrics and Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Frank A SimmenDepartment of Physiology & Biophysics, Department of Pediatrics and Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Rosalia C M SimmenDepartment of Physiology & Biophysics, Department of Pediatrics and Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA simmenrosalia@uams.edu.
Arkansas Children's Hospital · US

Funding

Arkansas Center for Clinical and Translational ResearchUL1TR000039 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI BECK, CORNELIA MARIE, JAMES, LAURA P · 2012 to 2014
$10.0M
Dietary Factors in Colon Cancer PreventionR01CA136493 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI SIMMEN, FRANK ALBERT · 2010 to 2014
$1.4M
NCATS NIH HHS 1 UL1TR000039NCI NIH HHS R01 CA136493NCI NIH HHS R01CA136493
6 · The paper itself

Abstract

Many adult chronic diseases are thought to be influenced during early life by maternal nutrition; however, the underlying mechanisms remain largely unknown. Obesity-related diseases may be due partly to high fat consumption. Herein, we evaluated mammary tumor risk in female mouse mammary tumor virus-Wnt-1 transgenic (Tg) offspring exposed to high-fat diet (HFD) or control diet (CD) (45% and 17% kcal from fat, respectively) during gestation and lactation, with CD provided to progeny at weaning. In Tg offspring, maternal HFD exposure increased mammary tumor incidence and decreased tumor latency without affecting tumor volume. Tumor risk was associated with higher tumor necrosis factor-α and insulin and altered oxidative stress biomarkers in sera and with early changes in mammary expression of genes linked to tumor promotion [interleukin 6 (Il6)] or inhibition [phosphatase and tensin homolog deleted on chromosome 10 (Pten), B-cell lymphoma 2 (Bcl2)]. Corresponding wild-type progeny exposed to maternal HFD displayed accelerated mammary development, higher mammary adiposity, increased insulin resistance and early changes in Pten, Bcl2 and Il6, than CD-exposed offspring. Dams-fed HFD showed higher serum glucose and oxidative stress biomarkers but comparable adiposity compared with CD-fed counterparts. In human breast cancer MCF-7 cells, sera from maternal HFD-exposed Tg offspring elicited changes in PTEN, BCL2 and IL6 gene expression, mimicking in vivo exposure; increased cell viability and mammosphere formation and induced measures [insulin receptor substrate-1 (IRS-1), IRS-2] of insulin sensitivity. Serum effects on IRS-1 were recapitulated by exogenous insulin and the PTEN-specific inhibitor SF1670. Hyperinsulinemia and PTEN loss-of-function may thus, couple maternal HFD exposure to enhanced insulin sensitivity via increased mammary IRS-1 expression in progeny, to promote breast cancer risk.

Indexed as

AnimalsAnimals, SucklingDiet, High-FatFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansLactationMaleMammary Glands, AnimalMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred C57BLMice, TransgenicOxidative StressTumor Suppressor ProteinsWnt1 ProteinWnt1 protein, mouse

Identifiers

PMID24832086
PMCPMC4146417
OpenAlexW2033878889

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.