Evidence map›Paper›PMID 30082828›Full record

ArticleScientific reports2018

ICAM1 expression is induced by proinflammatory cytokines and associated with TLS formation in aggressive breast cancer subtypes.

Stine L Figenschau, Erik Knutsen, Ilona Urbarova, Christopher Fenton, Bryan Elston, Maria Perander, Elin S Mortensen, Kristin A Fenton

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
6.7field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

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11 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

8 authors at 2 institutions in 1 country.

Stine L FigenschauRNA and Molecular Pathology Research group, Department of Medical Biology, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway.ORCID 0000-0002-3714-9998
Erik KnutsenRNA and Molecular Pathology Research group, Department of Medical Biology, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway.
Ilona UrbarovaTromsø University Proteomics Platform, Department of Medical Biology, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway.
Christopher FentonThe Microarray Platform, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway.
Bryan ElstonHistopath Diagnostic Specialists, Suite 201, 4 Drake Avenue, Building B Pinnacle Office Park, Macquarie Park, NSW, 2113, Australia.
Maria PeranderRNA and Molecular Pathology Research group, Department of Medical Biology, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway.
Elin S MortensenRNA and Molecular Pathology Research group, Department of Medical Biology, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway.
Kristin A FentonRNA and Molecular Pathology Research group, Department of Medical Biology, Faculty of Health Science, UiT - The Arctic University of Norway, N-9037, Tromsø, Norway. kristin.fenton@uit.no.ORCID 0000-0002-8356-2628
UiT The Arctic University of Norway · NOUniversity Hospital of North Norway · NO

Funding

Helse Nord RHF (Northern Norway Regional Health Authority) SFP1222-15Kreftforeningen (Norwegian Cancer Society) 2290738-2011
6 · The paper itself

Abstract

Intratumoral formation of tertiary lymphoid structures (TLS) within the tumor microenvironment is considered to be a consequence of antigen challenge during anti-tumor responses. Intracellular adhesion molecule 1 (ICAM1) has been implicated in a variety of immune and inflammatory responses, in addition to associate with triple negative breast cancer (TNBC). In this study, we detected TLS in the aggressive tumor phenotypes TNBC, HER2+ and luminal B, whereas the TLS negative group contained solely tumors of the luminal A subtype. We show that ICAM1 is exclusively expressed in TNBC and HER2 enriched subtypes known to be associated with inflammation and the formation of TLS. Furthermore, cell from normal mammary epithelium and breast cancer cell lines expressed ICAM1 upon stimulation with the proinflammatory cytokines TNFα, IL1β and IFNγ. ICAM1 overexpression was induced in MCF7, MDA-MB-468 and SK-BR-3 cells regardless of hormone receptor status. Taken together, our findings show that ICAM1 is expressed in aggressive subtypes of breast cancer and its expression is inducible by well-known proinflammatory cytokines. ICAM1 may be an attractive molecular target for TNBC, but further investigations elucidating the role of ICAM1 in targeted therapies have to take into consideration selective subtypes of breast cancer.

Indexed as

Breast NeoplasmsCell Line, TumorCytokinesErb-b2 Receptor Tyrosine KinasesFemaleHumansImmunohistochemistryIntercellular Adhesion Molecule-1MCF-7 CellsTertiary Lymphoid StructuresTriple Negative Breast NeoplasmsTumor MicroenvironmentCytokinesErb-b2 Receptor Tyrosine KinasesICAM1 protein, humanIntercellular Adhesion Molecule-1

Identifiers

PMID30082828
PMCPMC6079003
OpenAlexW2885369719

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.