Evidence mapPaperPMID 39457693Full record

ReviewBiomedicines2024

Insights into CSF-1R Expression in the Tumor Microenvironment.

Caterina Tomassetti, Gaia Insinga, Francesca Gimigliano, Andrea Morrione, Antonio Giordano, Emanuele Giurisato

Abstract readReview
In one paragraph

Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
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

34 citing papers in PubMed.

  1. Article
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  7. Drug allergy history predicts early progression-free survival benefit from PD-(L)1 inhibitors in advanced non-small cell lung cancer: a retrospective cohort study.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  8. Review
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  15. The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  16. Cancer Metastasis: Therapeutic Challenges and Opportunities.Medical oncology (Northwood, London, England) · 2025
    Review
  17. Review
  18. Article
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  20. Transcriptional Repression of CCL2 by KInternational journal of molecular sciences · 2025
    Article
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

6 authors.

Caterina TomassettiDepartment of Biotechnology Chemistry and Pharmacy, University of Siena, 53100 Siena, Italy.
Gaia InsingaDepartment of Mental and Physical Health and Preventive Medicine, University of Campania "Luigi Vanvitelli", 80138 Napoli, Italy.
Francesca GimiglianoDepartment of Mental and Physical Health and Preventive Medicine, University of Campania "Luigi Vanvitelli", 80138 Napoli, Italy.
Andrea MorrioneSbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Department of Biology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.ORCID 0000-0002-2319-7884
Antonio GiordanoDepartment of Medical Biotechnologies, University of Siena, 53100 Siena, Italy.ORCID 0000-0002-5959-016X
Emanuele GiurisatoDepartment of Biotechnology Chemistry and Pharmacy, University of Siena, 53100 Siena, Italy.ORCID 0000-0003-0598-6449

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The colony-stimulating factor 1 receptor (CSF-1R) plays a pivotal role in orchestrating cellular interactions within the tumor microenvironment (TME). Although the CSF-1R has been extensively studied in myeloid cells, the expression of this receptor and its emerging role in other cell types in the TME need to be further analyzed. This review explores the multifaceted functions of the CSF-1R across various TME cellular populations, including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), dendritic cells (DCs), cancer-associated fibroblasts (CAFs), endothelial cells (ECs), and cancer stem cells (CSCs). The activation of the CSF-1R by its ligands, colony-stimulating factor 1 (CSF-1) and Interleukin-34 (IL-34), regulates TAM polarization towards an immunosuppressive M2 phenotype, promoting tumor progression and immune evasion. Similarly, CSF-1R signaling influences MDSCs to exert immunosuppressive functions, hindering anti-tumor immunity. In DCs, the CSF-1R alters antigen-presenting capabilities, compromising immune surveillance against cancer cells. CSF-1R expression in CAFs and ECs regulates immune modulation, angiogenesis, and immune cell trafficking within the TME, fostering a pro-tumorigenic milieu. Notably, the CSF-1R in CSCs contributes to tumor aggressiveness and therapeutic resistance through interactions with TAMs and the modulation of stemness features. Understanding the diverse roles of the CSF-1R in the TME underscores its potential as a therapeutic target for cancer treatment, aiming at disrupting pro-tumorigenic cellular crosstalk and enhancing anti-tumor immune responses.

Indexed as

CAFscancer stem cellsCSF-1RECsMDSCsTAMstumor microenvironment

Identifiers

PMID39457693
PMCPMC11504891

What Socratic holds

Textmetadata
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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 Socratic graph.