Evidence map›Paper›PMID 26516917›Full record

ReviewCancers2015

The Interactions of Obesity, Inflammation and Insulin Resistance in Breast Cancer.

David P Rose, Peter J Gracheck, Linda Vona-Davis

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 4 pooled it
7.5field-weighted citation impact, top 2% 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

79 citing papers in PubMed, 4 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
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  4. Does dienogest influence the inflammatory response of endometriotic cells? A systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Pooled it
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19 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

David P RoseMary Babb Randolph Cancer Center,West Virginia University Health Sciences Center, Morgantown, WV 26506, USA. davidrosemd@hotmail.com.
Peter J GracheckMary Babb Randolph Cancer Center,West Virginia University Health Sciences Center, Morgantown, WV 26506, USA. pjgracheck@mix.wvu.edu.
Linda Vona-DavisMary Babb Randolph Cancer Center,West Virginia University Health Sciences Center, Morgantown, WV 26506, USA. lvdavis@hsc.wvu.edu.
West Virginia University · USWest Virginia University Hospitals · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Laura F. Gibson · 2012 to 2026
$81.0M
NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

Obese postmenopausal women have an increased breast cancer risk, the principal mechanism for which is elevated estrogen production by adipose tissue; also, regardless of menstrual status and tumor estrogen dependence, obesity is associated with biologically aggressive breast cancers. Type 2 diabetes has a complex relationship with breast cancer risk and outcome; coexisting obesity may be a major factor, but insulin itself induces adipose aromatase activity and estrogen production and also directly stimulates breast cancer cell growth and invasion. Adipose tissue inflammation occurs frequently in obesity and type 2 diabetes, and proinflammatory cytokines and prostaglandin E2 produced by cyclooxygenase-2 in the associated infiltrating macrophages also induce elevated aromatase expression. In animal models, the same proinflammatory mediators, and the chemokine monocyte chemoattractant protein-1, also stimulate tumor cell proliferation and invasion directly and promote tumor-related angiogenesis. We postulate that chronic adipose tissue inflammation, rather than body mass index-defined obesity per se, is associated with an increased risk of type 2 diabetes and postmenopausal estrogen-dependent breast cancer. Also, notably before the menopause, obesity and type 2 diabetes, or perhaps the associated inflammation, promote estrogen-independent, notably triple-negative, breast cancer development, invasion and metastasis by mechanisms that may involve macrophage-secreted cytokines, adipokines and insulin.

Indexed as

breast cancerinflammationinsulin

Identifiers

PMID26516917
PMCPMC4695883
OpenAlexW2101459489

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.