Evidence map›Paper›PMID 26392082›Full record

ArticleBreast cancer research : BCR2015

Expression of functional toll like receptor 4 in estrogen receptor/progesterone receptor-negative breast cancer.

Meliha Mehmeti, Roni Allaoui, Caroline Bergenfelz, Lao H Saal, Stephen P Ethier, Martin E Johansson, Karin Jirström, Karin Leandersson

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017
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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

8 authors at 2 institutions in 2 countries.

Meliha MehmetiCenter for Molecular Pathology, Department of Translational Medicine, Lund University, SUS Jan Waldenströmsgata 59, 20502, Malmö, Sweden. Meliha.Mehmeti@med.lu.se.
Roni AllaouiCenter for Molecular Pathology, Department of Translational Medicine, Lund University, SUS Jan Waldenströmsgata 59, 20502, Malmö, Sweden. Roni.Allaoui@med.lu.se.
Caroline BergenfelzCenter for Molecular Pathology, Department of Translational Medicine, Lund University, SUS Jan Waldenströmsgata 59, 20502, Malmö, Sweden. Caroline.Bergenfelz@med.lu.se.
Lao H SaalDivision of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden. lao.saal@med.lu.se.
Stephen P EthierDepartment of Pathology and Laboratory Medicine, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA. ethier@musc.edu.
Martin E JohanssonCenter for Molecular Pathology, Department of Translational Medicine, Lund University, SUS Jan Waldenströmsgata 59, 20502, Malmö, Sweden. Martin.Johansson@med.lu.se.
Karin JirströmDivision of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden. Karin.Jirstrom@med.lu.se.
Karin LeanderssonCenter for Molecular Pathology, Department of Translational Medicine, Lund University, SUS Jan Waldenströmsgata 59, 20502, Malmö, Sweden. Karin.Leandersson@med.lu.se.
Lund University · SEMUSC Hollings Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionToll-like receptors (TLRs) are a family of pattern recognition receptors that are expressed on cells of the innate immune system. The ligands can be pathogen derived (pathogen associated molecular patterns; PAMPs) or endogenous (damage associated molecular patterns; DAMPs) that when bound induces activation of nuclear factor kappa B (NF-κB) and transcription of pro-inflammatory genes. TLRs have also been discovered in various malignant cell types, but with unknown function.

methodsIn this study we performed a detailed analysis of TLR and co-receptor expression pattern and function in breast cancer. Expression patterns were examined using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) on three estrogen receptor-positive (ER(+)) and four estrogen receptor/progesterone receptor-negative (ER(-)/PR(-); ER/PR-negative) breast cancer cell lines, and a breast cancer cohort consisting of 144 primary breast cancer samples. The function was investigated using in vitro assays comprising PAMP/DAMP-stimulation, downstream signaling and TLR-silencing experiments.

resultsWe found that TLR4 was expressed in a biologically active form and responded to both PAMPs and DAMPs primarily in ER/PR-negative breast cancers. Stimulation of TLR2/4 in vitro induced expression of pro-inflammatory genes and a gene expression analysis of primary breast cancers showed a strong correlation between TLR4 expression and expression of pro-inflammatory mediators. In line with this, TLR4 protein expression correlated with a decreased survival.

conclusionsThese findings suggest that TLR4 is expressed in a functional form in ER/PR-negative breast cancers. Studies regarding TLR4-antagonist therapies should be focusing on ER/PR-negative breast cancer particularly.

Indexed as

Breast NeoplasmsCell Line, TumorFemaleGene ExpressionHumansMCF-7 CellsNF-kappa BReceptors, EstrogenReceptors, ProgesteroneSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4NF-kappa BReceptors, EstrogenReceptors, ProgesteroneTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID26392082
PMCPMC4578669
OpenAlexW2136324562

What OpenQuestion holds

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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.