ArticleJCI insight2018
CSF1R-dependent myeloid cells are required for NK‑mediated control of metastasis.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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.
Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Pathophysiological roles of monocytes and macrophages in cancer.Nature reviews. Immunology · 2026Review
- Macrophage Plasticity in Cancer Therapy: Function, Timing, and Tradeoffs.International journal of molecular sciences · 2026Review
- Targeting macrophage-driven NK cell immunosuppression to improve cancer immunotherapy.Journal for immunotherapy of cancer · 2026Review
- Tissue localization of natural killer cells dictates surveillance of lung metastasis.Nature communications · 2025Article
- Treatment Resistant Persister Cells Exploit Macrophage Lipid Metabolism to Sustain Glioblastoma Growth.bioRxiv : the preprint server for biology · 2025Article
- Targeting Triple NK Cell Suppression Mechanisms: A Comprehensive Review of Biomarkers in Pancreatic Cancer Therapy.International journal of molecular sciences · 2025Review
- Enhancing natural killer cell anti-tumour activity through macrophage manipulation.Frontiers in immunology · 2025Review
- Insights into CSF-1R Expression in the Tumor Microenvironment.Biomedicines · 2024Review
- Article
- Mechanistic studies of tumor-associated macrophage immunotherapy.Frontiers in immunology · 2024Review
- Tumour-associated macrophages as a potential target to improve natural killer cell-based immunotherapies.Essays in biochemistry · 2023Article
- Understanding NK cell biology for harnessing NK cell therapies: targeting cancer and beyond.Frontiers in immunology · 2023Review
- Limitations of PLX3397 as a microglial investigational tool: peripheral and off-target effects dictate the response to inflammation.Frontiers in immunology · 2023Article
- S-nitrosylation of CSF1 receptor increases the efficacy of CSF1R blockage against prostate cancer.Cell death & disease · 2022Article
- Macrophages in ovarian cancer and their interactions with monoclonal antibody therapies.Clinical and experimental immunology · 2022Review
- Spatial transcriptomics of macrophage infiltration in non-small cell lung cancer reveals determinants of sensitivity and resistance to anti-PD1/PD-L1 antibodies.Journal for immunotherapy of cancer · 2022Article
- Loss of the intracellular enzyme QPCTL limits chemokine function and reshapes myeloid infiltration to augment tumor immunity.Nature immunology · 2022Article
- MEK1/2 inhibition transiently alters the tumor immune microenvironment to enhance immunotherapy efficacy against head and neck cancer.Journal for immunotherapy of cancer · 2022Article
- Conventional NK cells and tissue-resident ILC1s join forces to control liver metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Immune Circuits to Shape Natural Killer Cells in Cancer.Cancers · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloid leukocytes are essentially involved in both tumor progression and control. We show that neo-adjuvant treatment of mice with an inhibitor of CSF1 receptor (CSF1R), a drug that is used to deplete tumor-associated macrophages, unexpectedly promoted metastasis. CSF1R blockade indirectly diminished the number of NK cells due to a paucity of myeloid cells that provide the survival factor IL-15 to NK cells. Reduction of the number of NK cells resulted in increased seeding of metastatic tumor cells to the lungs but did not impact on progression of established metastases. Supplementation of mice treated with CSF1R-inhibitor with IL-15 restored numbers of NK cells and diminished metastasis. Our data suggest that CSF1R blockade should be combined with administration of IL-15 to reduce the risk of metastasis.
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What OpenQuestion holds
Registered trials
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.