Evidence map›Paper›PMID 32370743›Full record

ArticleBMC cancer2020

MiR-18a and miR-18b are expressed in the stroma of oestrogen receptor alpha negative breast cancers.

Nina Gran Egeland, Kristin Jonsdottir, Miriam Ragle Aure, Kristine Sahlberg, Vessela N Kristensen, Deirdre Cronin-Fenton, Ivar Skaland, Einar Gudlaugsson, Jan P A Baak, Emiel A M Janssen

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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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

10 authors at 6 institutions in 2 countries.

Nina Gran EgelandDepartment of Pathology, Stavanger University Hospital, Box 8100, 4068, Stavanger, Norway.
Kristin JonsdottirDepartment of Pathology, Stavanger University Hospital, Box 8100, 4068, Stavanger, Norway. kristin.jonsdottir@sus.no.
Miriam Ragle AureDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Kristine SahlbergDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Vessela N KristensenDepartment of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Deirdre Cronin-FentonDepartment of Clinical Epidemiology, Aarhus University, Aarhus, Denmark.
Ivar SkalandDepartment of Pathology, Stavanger University Hospital, Box 8100, 4068, Stavanger, Norway.
Einar GudlaugssonDepartment of Pathology, Stavanger University Hospital, Box 8100, 4068, Stavanger, Norway.
Jan P A BaakDepartment of Pathology, Stavanger University Hospital, Box 8100, 4068, Stavanger, Norway.
Emiel A M JanssenDepartment of Pathology, Stavanger University Hospital, Box 8100, 4068, Stavanger, Norway.
Stavanger University Hospital · NOAarhus University · DKAkershus University Hospital · NOOslo University Hospital · NOUniversity of Stavanger · NOVestre Viken Hospital Trust · NO

Funding

Folke Hermansen Foundation 2013Folke Hermansen Foundation 2014Helse Sør-Øst RHF 2014021Helse Vest Regionalt Helseføretak 911790
6 · The paper itself

Abstract

backgroundPreviously, we have shown that miR-18a and miR-18b gene expression strongly correlates with high proliferation, oestrogen receptor -negativity (ER

methodsWe investigated the expression and localization of miR-18a and -18b in formalin fixed paraffin embedded (FFPE) tissue from lymph node negative breast cancers (n = 40), by chromogenic in situ hybridization (CISH). The expression level and in situ localization of miR-18a and -18b was assessed with respect to the presence of tumour infiltrating lymphocytes (TILs) and immunohistochemical markers for ER, CD4, CD8, CD20, CD68, CD138, PAX5 and actin. Furthermore, in two independent breast cancer cohorts (94 and 377 patients) the correlation between miR-18a and -18b expression and the relative quantification of 22 immune cell types obtained from the CIBERSORT tool was assessed.

resultsCISH demonstrated distinct and specific cytoplasmic staining for both miR-18a and miR-18b, particularly in the intratumoural stroma and the stroma surrounding the tumour margin. Staining by immunohistochemistry revealed some degree of overlap of miR-18a and -18b with CD68 (monocytes/macrophages), CD138 (plasma cells) and the presence of high percentages of TILs. CIBERSORT analysis showed a strong correlation between M1-macrophages and CD4+ memory activated T-cells with mir-18a and -18b.

conclusionsOur study demonstrates that miR-18a and miR-18b expression is associated with ER- breast tumours that display a high degree of inflammation. This expression is potentially associated specifically with macrophages. These results suggest that miR-18a and miR-18b may play a role in the systemic immunological response in ER

Indexed as

Biomarkers, TumorBreast NeoplasmsCohort StudiesDatabases, GeneticEstrogen Receptor alphaFemaleGene Expression Regulation, NeoplasticHumansLymphocytes, Tumor-InfiltratingMacrophagesMicroRNAsMiddle AgedStromal CellsBiomarkers, TumorESR1 protein, humanEstrogen Receptor alphaMicroRNAsMIRN18A microRNA, humanMIRN18 microRNA, humanBreast cancerIn situ hybridizationMacrophagesmicroRNATumour associated macrophages (TAM)Tumour microenvironment

Identifiers

PMID32370743
PMCPMC7201801
OpenAlexW3023149247

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.