Evidence map›Paper›PMID 21372033›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2011

Obesity is associated with inflammation and elevated aromatase expression in the mouse mammary gland.

Kotha Subbaramaiah, Louise R Howe, Priya Bhardwaj, Baoheng Du, Claudia Gravaghi, Rhonda K Yantiss, Xi Kathy Zhou, Victoria A Blaho, Timothy Hla, Peiying Yang and 3 more

RetractedOpen access · bronzeAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 215 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed, 5 pooled it
28.4field-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

215 citing papers in PubMed, 5 syntheses or guidelines pooled it, 362 citations in OpenAlex.

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  19. Targeting adipocyte-immune cell crosstalk to control breast cancer progression.Journal of cancer research and clinical oncology · 2023
    Review
  20. Review

155 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Kotha SubbaramaiahDepartment of Medicine and Weill Cornell Cancer Center, New York, NY 10065, USA. ksubba@med.cornell.edu
Louise R Howe
Priya Bhardwaj
Baoheng Du
Claudia Gravaghi
Rhonda K Yantiss
Xi Kathy Zhou
Victoria A Blaho
Timothy Hla
Peiying Yang
Levy Kopelovich
Clifford A Hudis
Andrew J Dannenberg
Cornell University · USMemorial Sloan Kettering Cancer Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

Collaborative Program in Nutrition and Cancer Prevention (PNCP)R25CA105012 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CUNNINGHAM-RUNDLES, SUSANNA · 2006 to 2010
$2.3M
NCI NIH HHS N01 CN043302NCI NIH HHS N01-CN-43302NCI NIH HHS R25 CA105012NCI NIH HHS R25CA105012
6 · The paper itself

Abstract

Elevated circulating estrogen levels are associated with increased risk of breast cancer in obese postmenopausal women. Following menopause, the biosynthesis of estrogens through CYP19 (aromatase)-mediated metabolism of androgen precursors occurs primarily in adipose tissue, and the resulting estrogens are then secreted into the systemic circulation. The potential links between obesity, inflammation, and aromatase expression are unknown. In both dietary and genetic models of obesity, we observed necrotic adipocytes surrounded by macrophages forming crown-like structures (CLS) in the mammary glands and visceral fat. The presence of CLS was associated with activation of NF-κB and increased levels of proinflammatory mediators (TNF-α, IL-1β, Cox-2), which were paralleled by elevated levels of aromatase expression and activity in the mammary gland and visceral fat of obese mice. Analyses of the stromal-vascular and adipocyte fractions of the mammary gland suggested that macrophage-derived proinflammatory mediators induced aromatase and estrogen-dependent gene expression (PR, pS2) in adipocytes. Saturated fatty acids, which have been linked to obesity-related inflammation, stimulated NF-κB activity in macrophages leading to increased levels of TNF-α, IL-1β, and Cox-2, each of which contributed to the induction of aromatase in preadipocytes. The discovery of the obesity → inflammation → aromatase axis in the mammary gland and visceral fat and its association with CLS may provide insight into mechanisms underlying the increased risk of hormone receptor-positive breast cancer in obese postmenopausal women, the reduced efficacy of aromatase inhibitors in the treatment of breast cancer in these women, and their generally worse outcomes. The presence of CLS may be a biomarker of increased breast cancer risk or poor prognosis.

Indexed as

Gene Expression Regulation, NeoplasticInflammationAdipocytesAnimalsAromataseBiomarkers, TumorDisease Models, AnimalFatty AcidsFemaleHumansMammary Glands, AnimalMammary Neoplasms, AnimalMiceMice, Inbred C57BLObesityAromataseBiomarkers, TumorFatty Acids

Identifiers

PMID21372033
PMCPMC3071249
OpenAlexW2145533373

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.