Evidence map›Paper›PMID 24316750›Full record

ArticleScientific reports2013

IL-17A is produced by breast cancer TILs and promotes chemoresistance and proliferation through ERK1/2.

Stéphanie Cochaud, Jérôme Giustiniani, Clémence Thomas, Emilie Laprevotte, Christian Garbar, Aude-Marie Savoye, Hervé Curé, Corinne Mascaux, Gilles Alberici, Nathalie Bonnefoy and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

88 citing papers in PubMed, 143 citations in OpenAlex.

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  9. The IL-17 family in diseases: from bench to bedside.Signal transduction and targeted therapy · 2023
    Review
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  12. Pathogens (Basel, Switzerland) · 2023
    Article
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28 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

13 authors at 5 institutions in 1 country.

Stéphanie Cochaud1] Institut National de la Santé et de la Recherche Médicale (INSERM) UMR-S 976; Université Paris Diderot, Sorbonne Paris Cité, Laboratoire Immunologie Dermatologie & Oncologie, F-75475, Paris, France [2].
Jérôme Giustiniani
Clémence Thomas
Emilie Laprevotte
Christian Garbar
Aude-Marie Savoye
Hervé Curé
Corinne Mascaux
Gilles Alberici
Nathalie Bonnefoy
Jean-François Eliaou
Armand Bensussan
Jeremy Bastid
Institut Jean Godinot · FROREGA Biotech (France) · FRCEA Valduc · FRInserm · FRSorbonne Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proinflammatory cytokine Interleukin 17A (hereafter named IL-17A) or IL-17A producing cells are elevated in breast tumors environment and correlate with poor prognosis. Increased IL-17A is associated with ER(-) or triple negative tumors and reduced Disease Free Survival. However, the pathophysiological role of IL-17A in breast cancer remains unclear although several studies suggested its involvement in cancer cell dissemination. Here we demonstrated that a subset of breast tumors is infiltrated with IL-17A-producing cells. Increased IL-17A seems mainly associated to ER(-) and triple negative/basal-like tumors. Isolation of tumor infiltrating T lymphocytes (TILs) from breast cancer biopsies revealed that these cells secreted significant amounts of IL-17A. We further established that recombinant IL-17A recruits the MAPK pathway by upregulating phosphorylated ERK1/2 in human breast cancer cell lines thereby promoting proliferation and resistance to conventional chemotherapeutic agents such as docetaxel. We also confirmed here that recombinant IL-17A stimulates migration and invasion of breast cancer cells as previously reported. Importantly, TILs also induced tumor cell proliferation, chemoresistance and migration and treatment with IL-17A-neutralizing antibodies abrogated these effects. Altogether these results demonstrated the pathophysiological role of IL-17A-producing cell infiltrate in a subset of breast cancers. Therefore, IL-17A appears as potential therapeutic target for breast cancer.

Indexed as

Drug Resistance, NeoplasmMAP Kinase Signaling SystemAntineoplastic AgentsBiopsyBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDocetaxelFemaleHumansInterleukin-17Lymphocytes, Tumor-InfiltratingMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, EstrogenAntineoplastic AgentsDocetaxelInterleukin-17Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Receptors, EstrogenTaxoids

Identifiers

PMID24316750
PMCPMC3856404
OpenAlexW2140374399

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.