Evidence map›Paper›PMID 22301780›Full record

ReviewMolecular endocrinology (Baltimore, Md.)2012

Minireview: Inflammation: an instigator of more aggressive estrogen receptor (ER) positive breast cancers.

Sarah C Baumgarten, Jonna Frasor

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular endocrinology (Baltimore, Md.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 1 pooled it
8.5field-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

103 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.

  1. Pooled it
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  9. Contribution of Prediagnostic Host Factors to Shaping the Stromal Microenvironment of Breast Cancer among Sub-Saharan African Women.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025
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43 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

2 authors at 1 institution in 1 country.

Sarah C BaumgartenDepartment of Physiology and Biophysics, University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, IL 60612, USA.
Jonna Frasor
University of Illinois Chicago · US

Funding

TRAINING IN CELLULAR SIGNALLING IN THE CARDIOVASCULAR SYT32HL007692 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1990 to 2014
$8.5M
Crosstalk between estrogen receptor and NFkB in target gene regulationR01CA130932 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FRASOR, JONNA · 2009 to 2013
$1.5M
NCI NIH HHS CA130932-3NCI NIH HHS R01 CA130932NHLBI NIH HHS T32 HL007692NHLBI NIH HHS T32 HL07692-21
6 · The paper itself

Abstract

Approximately 75% of breast tumors express the estrogen receptor (ER), and women with these tumors will receive endocrine therapy. Unfortunately, up to 50% of these patients will fail ER-targeted therapies due to either de novo or acquired resistance. ER-positive tumors can be classified based on gene expression profiles into Luminal A- and Luminal B-intrinsic subtypes, with distinctly different responses to endocrine therapy and overall patient outcome. However, the underlying biology causing this tumor heterogeneity has yet to become clear. This review will explore the role of inflammation as a risk factor in breast cancer as well as a player in the development of more aggressive, therapy-resistant ER-positive breast cancers. First, breast cancer risk factors, such as obesity and mammary gland involution after pregnancy, which can foster an inflammatory microenvironment within the breast, will be described. Second, inflammatory components of the tumor microenvironment, including tumor-associated macrophages and proinflammatory cytokines, which can act on nearby breast cancer cells and modulate tumor phenotype, will be explored. Finally, activation of the nuclear factor κB (NF-κB) pathway and its cross talk with ER in the regulation of key genes in the promotion of more aggressive breast cancers will be reviewed. From these multiple lines of evidence, we propose that inflammation may promote more aggressive ER-positive tumors and that combination therapy targeting both inflammation and estrogen production or actions could benefit a significant portion of women whose ER-positive breast tumors fail to respond to endocrine therapy.

Indexed as

AnimalsBreast NeoplasmsCytokinesFemaleGene ExpressionGene Expression Regulation, NeoplasticHumansInflammationPregnancyReceptor Cross-TalkReceptors, EstrogenRisk FactorsCytokinesReceptors, Estrogen

Identifiers

PMID22301780
PMCPMC3286192
OpenAlexW2074143255

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.