Evidence map›Paper›PMID 40037357›Full record

ArticleCell reports. Medicine2025

Inflammatory reprogramming of the solid tumor microenvironment by infiltrating clonal hematopoiesis is associated with adverse outcomes.

Marco M Buttigieg, Caitlyn Vlasschaert, Alexander G Bick, Robert J Vanner, Michael J Rauh

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

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  13. Demystifying the diagnosis and management of ICUS, CHIP, and CCUS.Hematology. American Society of Hematology. Education Program · 2025
    Review
  14. Article
  15. Clonal Hematopoiesis of Indeterminate Potential Influences Breast Cancer Outcomes in a Genotype-Specific Manner.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  16. Ageing, immune fitness and cancer.Nature reviews. Cancer · 2025
    Review
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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

5 authors.

Marco M ButtigiegDepartment of Pathology & Molecular Medicine, Queen's University, Kingston, ON, Canada.
Caitlyn VlasschaertDepartment of Medicine, Queen's University, Kingston, ON, Canada.
Alexander G BickVanderbilt Genetics Institute, Vanderbilt University School of Medicine, Nashville, TN, USA; Division of Genetic Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
Robert J VannerDepartment of Medical Oncology and Hematology, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada; Institute of Medical Science, Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada. Electronic address: robert.vanner@uhn.ca.
Michael J RauhDepartment of Pathology & Molecular Medicine, Queen's University, Kingston, ON, Canada; Department of Medicine, Queen's University, Kingston, ON, Canada. Electronic address: rauhm@queensu.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal hematopoiesis (CH)-the expansion of somatically mutated hematopoietic cells-is common in solid cancers. CH is associated with systemic inflammation, but its impact on tumor biology is underexplored. Here, we report the effects of CH on the tumor microenvironment (TME) using 1,550 treatment-naive patient samples from the Clinical Proteomics Tumor Analysis Consortium (CPTAC) cohort. CH is present in 18.3% of patients, with one-third of CH mutations also detectable in tumor-derived DNA from the same individual (CH-Tum), reflecting CH-mutant leukocyte infiltration. Across cancers, the presence of CH-Tum is associated with worse survival outcomes. Molecular analyses reveal an association between CH-Tum and an immune-rich, inflammatory TME that is notably distinct from age-related gene expression changes. These effects are most prominent in glioblastoma, where CH correlates with pronounced macrophage infiltration, inflammation, and an aggressive, mesenchymal phenotype. Our findings demonstrate that CH shapes the TME, with potential applications as a biomarker in precision oncology.

Indexed as

Clonal HematopoiesisInflammationNeoplasmsTumor MicroenvironmentFemaleHumansMaleMutationcancerclonal hematopoiesisclonal hematopoiesis of indeterminate potentialCPTACglioblastomaimmunityinflammationprecision oncologyTCGAtumor microenvironment

Identifiers

PMID40037357
PMCPMC11970403

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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.