Evidence map›Paper›PMID 23958744›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

Molecular pathways: adipose inflammation as a mediator of obesity-associated cancer.

Louise R Howe, Kotha Subbaramaiah, Clifford A Hudis, Andrew J Dannenberg

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
202citing papers in PubMed, 9 pooled it
23.0field-weighted citation impact, top 1% 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

202 citing papers in PubMed, 9 syntheses or guidelines pooled it, 336 citations in OpenAlex.

  1. Pooled it
  2. Leptin signaling in breast cancer and its crosstalk with peroxisome proliferator-activated receptors α and γ.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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142 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

4 authors at 2 institutions in 1 country.

Louise R HoweAuthors' Affiliations: Departments of Cell & Developmental Biology and Medicine, Weill Cornell Medical College; and Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York.
Kotha Subbaramaiah
Clifford A Hudis
Andrew J Dannenberg
Cornell University · USMemorial Sloan Kettering Cancer Center · US

Funding

Targeting the Obesity-Inflammation-COX-Aromatase Axis to Lower Breast Cancer RiskR01CA154481 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DANNENBERG, ANDREW JESS · 2011 to 2015
$1.7M
NCI NIH HHS CA154481NCI NIH HHS R01 CA154481
6 · The paper itself

Abstract

The increasing rate of obesity worldwide is predicted to be associated with a surge in diseases. Notably, obesity has been linked to approximately 20% of cancer cases in the United States; obesity is associated with both increased risk and worse outcomes after diagnosis. Altered levels of circulating factors are strongly implicated, including insulin, insulin-like growth factor 1, leptin, adiponectin, and interleukin-6 (IL-6). In addition, increasing attention has focused on the consequences of local adipose inflammation. Inflammatory foci characterized by crown-like structures consisting of dead adipocytes encircled by macrophages occur in white adipose depots, including the breast tissue, of most overweight and obese women. Saturated fatty acids, released as a consequence of obesity-associated lipolysis, induce macrophage activation via Toll-like receptor 4, thereby stimulating NF-κB signaling. This, in turn, activates transcription of proinflammatory genes including COX-2, IL-6, IL-1β, and TNFα. Elevated levels of proinflammatory mediators cause both local and systemic effects. Of particular relevance with regard to breast cancer is increased transcription of the CYP19 gene encoding aromatase, the rate-limiting enzyme for estrogen synthesis. Notably, this obesity-inflammation-aromatase axis provides a plausible explanation for increased rates of postmenopausal, hormone receptor-positive breast cancer associated with obesity and hence may offer targets for interventions to attenuate risk or improve prognosis. Potential approaches include weight reduction, exercise, and suppression of obesity-driven signaling pathways using pharmaceutical or dietary agents. A key future goal is to identify biomarkers that accurately report adipose inflammation, both for identification of at-risk individuals and to assess the efficacy of interventions. Clin Cancer Res; 19(22); 6074-83. ©2013 AACR.

Indexed as

AdipocytesAdipose TissueAromataseBreast NeoplasmsCyclooxygenase 2FemaleHumansInflammationInterleukin-1betaInterleukin-6Macrophage ActivationMacrophagesNF-kappa BObesityToll-Like Receptor 4Tumor Necrosis Factor-alphaAromataseCyclooxygenase 2IL6 protein, humanInterleukin-1betaInterleukin-6NF-kappa BPTGS2 protein, humanTLR4 protein, humanToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID23958744
PMCPMC3891839
OpenAlexW2118148875

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.