Evidence map›Paper›PMID 41870007›Full record

ArticleOncoimmunology2026

Immune cell clustering identifies a CD163⁺/CSF1R⁺ macrophage and neutrophil-enriched phenotype with distinct biological signatures and poor prognosis in angiosarcoma.

Adrian Georg Simon, Bastian Grothey, Su Ir Lyu, David Stahl, Lars Mortimer Schiffmann, Christiane Josephine Bruns, Peer Eysel, Reinhard Buettner, Roland Tillmann Ullrich, Alexander Quaas

Abstract read
In one paragraph

Article in Oncoimmunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Virtual single-cell perturbation and genetic causal inference revealJournal of cell communication and signaling · 2026
    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

10 authors.

Adrian Georg SimonInstitute of Pathology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID 0000-0002-2709-863X
Bastian GrotheyInstitute of Pathology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Su Ir LyuInstitute of Pathology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
David StahlDepartment I of Internal Medicine/Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Lars Mortimer SchiffmannDepartment of General, Visceral, Thoracic and Transplant Surgery, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Christiane Josephine BrunsDepartment of General, Visceral, Thoracic and Transplant Surgery, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Peer EyselDepartment for Orthopedics and Trauma Surgery, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Reinhard BuettnerInstitute of Pathology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Roland Tillmann UllrichDepartment I of Internal Medicine/Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.
Alexander QuaasInstitute of Pathology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor immune microenvironment (TIME) influences tumor biology and therapeutic response, yet its composition and clinical relevance in angiosarcoma, an ultrarare and aggressive sarcoma with a dismal prognosis, remain poorly defined. To address this gap, we comprehensively profiled the TIME of 63 angiosarcomas (AS), including primary cutaneous, secondary, and visceral subtypes, with a focus on colony-stimulating factor 1 receptor (CSF1R)-expressing tumor-associated macrophages (TAMs). Using conventional and multiplex immunohistochemistry with quantitative analysis, we found that CD68⁺/CD163⁺ (M2-like) TAMs predominated across all AS subtypes. The enrichment of CD68⁺/CD163⁺/CSF1R⁺ TAMs was strongly associated with shorter overall and disease-free survival. Unsupervised clustering revealed three immune phenotypes, among which a CSF1R-high macrophage/neutrophil-enriched cluster was independently associated with poor overall survival. Proteomic profiling of these high-risk angiosarcomas within this cluster demonstrated upregulation of oxidative phosphorylation, angiogenesis, and neutrophil-associated pathways, alongside downregulation of extracellular matrix organization, indicating a metabolically distinct and immunologically myeloid-driven tumor state and immune phenotype. These findings identify CSF1R⁺ macrophage enrichment as a defining feature of high-risk angiosarcoma and suggest that improved biological understanding of the CSF1R axis may allow additional immunomodulatory therapeutic strategies in this rare and aggressive malignancy.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticHemangiosarcomaMacrophagesNeutrophilsReceptors, Cell SurfaceReceptors, Granulocyte-Macrophage Colony-Stimulating FactorTumor-Associated MacrophagesAgedCD163 AntigenCluster AnalysisFemaleHumansMaleMiddle AgedPhenotypeAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCSF1R protein, humanReceptor, Macrophage Colony-Stimulating FactorReceptors, Cell SurfaceReceptors, Granulocyte-Macrophage Colony-Stimulating Factorcolony-stimulating factor 1 (CSF1)colony-stimulating factor 1 receptor (CSF1R)intratumoral macrophagessoft tissue sarcomatumor immune microenvironment (TIME)Tumor microenvironment

Identifiers

PMID41870007
PMCPMC13011603

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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.