Evidence map›Paper›PMID 40702585›Full record

ArticleGenome medicine2025

Epigenomic preconditioning of peripheral monocytes determines their transcriptional response to the tumor microenvironment.

Máté Kiss, Laszlo Halasz, Eva Hadadi, Wilhelm K Berger, Petros Tzerpos, Szilard Poliska, Daliya Kancheva, Aurélie Gabriel, Romina Mora Barthelmess, Ayla Debraekeleer and 9 more

Abstract read
In one paragraph

Article in Genome medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  5. Review
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  9. Observational
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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

19 authors.

Máté Kiss *Myeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium. mate.kiss@unige.ch.
Laszlo Halasz *Departments of Medicine and Biomedical Engineering, Johns Hopkins University School of Medicine, Institute for Fundamental Biomedical Research, Johns Hopkins All Children's Hospital, St. Petersburg, FL, USA.
Eva Hadadi *Myeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium.
Wilhelm K BergerDepartments of Medicine and Biomedical Engineering, Johns Hopkins University School of Medicine, Institute for Fundamental Biomedical Research, Johns Hopkins All Children's Hospital, St. Petersburg, FL, USA.
Petros TzerposDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Szilard PoliskaDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Daliya KanchevaMyeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium.
Aurélie GabrielDepartment of Oncology, Ludwig Institute for Cancer Research Lausanne, University of Lausanne, Lausanne, Switzerland.
Romina Mora BarthelmessMyeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium.
Ayla DebraekeleerLaboratory of Cellular and Molecular Immunology, Brussels Center for Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Jan BrughmansLaboratory of Cellular and Molecular Immunology, Brussels Center for Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Yvon ElkrimMyeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium.
Liesbet MartensData Mining and Modeling for Biomedicine Group, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Yvan SaeysData Mining and Modeling for Biomedicine Group, VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Bence DanielGenentech, South San Francisco, CA, USA.
Zsolt CzimmererInstitute of Genetics, HUN-REN Biological Research Centre, Szeged, Hungary.
Damya Laoui *Laboratory of Cellular and Molecular Immunology, Brussels Center for Immunology, Vrije Universiteit Brussel, Brussels, Belgium.
Laszlo Nagy *Departments of Medicine and Biomedical Engineering, Johns Hopkins University School of Medicine, Institute for Fundamental Biomedical Research, Johns Hopkins All Children's Hospital, St. Petersburg, FL, USA.
Jo A Van Ginderachter *Myeloid Cell Immunology Lab, VIB Center for Inflammation Research, Brussels, Belgium. jo.van.ginderachter@vub.be.

Funding

Nuclear receptor, PPARg in macrophage polarization, hyperinflammatory gene expression and lung injuryR01HL170426 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Laszlo Nagy · 2024 to 2026
$1.9M
Fonds Wetenschappelijk Onderzoek 12Y1922NJános Bolyai Research Scholarship BO/00594/22/8National Research, Development and Innovation Office 2023-1.1.1-PIACI_FÓKUSZ-2024-00036, K145994National Research, Development and Innovation Office TKP2021-NKTA-34NHLBI NIH HHS R01 HL170426NIH HHS HL170426Stichting Tegen Kanker F/2024/2625
6 · The paper itself

Abstract

backgroundMonocytes are recruited to tumors and undergo transcriptional reprogramming resulting in tumor-promoting functions. Epigenomic features, such as post-translational modification of histones and chromatin accessibility, are key determinants of transcription factor binding and thereby play an important role in controlling transcriptional responses to the tissue environment. It remains unknown whether systemic tumor-associated signals could alter the epigenomic landscape of peripheral monocytes before they reach the tumor, thus shaping their subsequent response to the tumor microenvironment.

methodsWe used a combination of genome-wide assays for chromatin accessibility and multiple histone modifications (H3K4me1, H3K4me3, H3K27ac) in a mouse tumor model to investigate changes in the epigenomic landscape of peripheral monocytes. We then integrated these epigenomic data with transcriptomic data to link altered regulatory elements to gene expression changes in monocytes occurring in the periphery or during tumor infiltration.

resultsWe found that tumor-induced systemic inflammation was associated with transcriptional and epigenomic preconditioning of peripheral monocytes. The distal tumor caused extensive remodeling of both H3K4me3

conclusionsThese results suggest that cancer-associated remodeling of the epigenomic landscape in peripheral monocytes can shape the gene expression programs they acquire in the tumor, highlighting the role of the epigenome in redirecting monocyte function to support cancer progression.

Indexed as

Epigenesis, GeneticEpigenomicsMonocytesNeoplasmsTranscription, GeneticTumor MicroenvironmentAnimalsChromatinGene Expression Regulation, NeoplasticHistone CodeHistonesHumansMicePromoter Regions, GeneticChromatinHistonesCancerEnhancerEpigenomeHistoneMonocyteTranscriptome

Identifiers

PMID40702585
PMCPMC12285133

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.