Evidence map›Paper›PMID 29872578›Full record

ArticleOncoimmunology

Tumor-associated macrophages in human breast cancer produce new monocyte attracting and pro-angiogenic factor YKL-39 indicative for increased metastasis after neoadjuvant chemotherapy.

Tengfei Liu, Irina Larionova, Nikolay Litviakov, Vladimir Riabov, Marina Zavyalova, Matvey Tsyganov, Mikhail Buldakov, Bin Song, Kondaiah Moganti, Polina Kazantseva and 6 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 74 citations in OpenAlex.

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  13. CD8Frontiers in immunology · 2024
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  20. Clever-1 positive macrophages in breast cancer.Breast cancer research and treatment · 2022
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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

16 authors at 4 institutions in 2 countries.

Tengfei LiuDepartment of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Mannheim, Germany.
Irina LarionovaLaboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia.
Nikolay LitviakovLaboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia.
Vladimir RiabovDepartment of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Mannheim, Germany.
Marina ZavyalovaLaboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia.
Matvey TsyganovCancer Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
Mikhail BuldakovLaboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia.
Bin SongDepartment of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Mannheim, Germany.
Kondaiah MogantiDepartment of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Mannheim, Germany.
Polina KazantsevaCancer Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
Elena SlonimskayaCancer Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
Elisabeth KremmerInstitute of Molecular Immunology, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Munich, Germany.
Andrew FlatleyInstitute of Molecular Immunology, Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Munich, Germany.
Harald KlüterDepartment of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Mannheim, Germany.
Nadezhda CherdyntsevaLaboratory for Translational Cellular and Molecular Biomedicine, Tomsk State University, Tomsk, Russia.
Julia KzhyshkowskaDepartment of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology, Mannheim, Germany.
Russian Academy of Sciences · RUHeidelberg University · DEHelmholtz Zentrum München · DENational Research Tomsk State University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In breast cancer, the tumor microenvironment plays a critical role in the tumor progression and responses to therapy. Tumor-associated macrophages (TAMs) are major innate immune cells in tumor microenvironment that regulate intratumoral immunity and angiogenesis by secretion of cytokines, growth factors as well as chitinase-like proteins (CLPs), that combine properties of cytokines and growth factors. YKL-39 is a chitinase-like protein found in human and absent in rodents, and its expression in TAMs and role in breast cancer progression was not studied to date. Here for the first time we demonstrate that YKL-39 is expressed on TAMs, predominantly positive for stabilin-1, but not by malignant cells or other stromal cells in human breast cancer. TGF-beta in combination with IL-4, but not IL-4 alone was responsible of the stimulation of the production of YKL-39 in human primary macrophages. Mechanistically, stabilin-1 directly interacted with YKL-39 and acted as sorting receptor for targeting YKL-39 into the secretory pathway. Functionally, purified YKL-39 acted as a strong chemotactic factor for primary human monocytes, and induced angiogenesis in vitro. Elevated levels of YKL-39 expression in tumors after neoadjuvant chemotherapy (NAC) were predictive for increased risk of distant metastasis and for poor response to NAC in patients with nonspecific invasive breast carcinoma. Our findings suggest YKL-39 as a novel therapeutic target, and blocking of its activity can be combined with NAC in order to reduce the risk of metastasis in breast cancer patients.

Indexed as

angiogenesisbreast cancerchemotaxischitinase-like proteinmonocyteneoadjuvant chemotherapytumor-associated macrophageYKL-39

Identifiers

PMID29872578
PMCPMC5980380
OpenAlexW2794152018

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.