ArticleiScience2025
Targeting the IL34-CSF1R axis improves metastatic renal cell carcinoma therapy outcome via immune-vascular crosstalk regulation.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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.
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Who cites it
1 citing paper in PubMed.
- Recent progress on tyrosine kinase inhibitors resistance in renal cell carcinoma: another brick in the wall?Cancer drug resistance (Alhambra, Calif.) · 2025Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current therapies ultimately fail to eradicate metastatic renal cell carcinoma (RCC). Validated biomarkers and a better understanding of the mechanisms causing therapy resistance are still needed. Here we demonstrate that interleukin-34 (IL34) is associated with poor prognosis, metastasis, and therapy resistance in RCC. In mice, single-nucleus RNA sequencing and phenotyping reveal that the IL34-enriched tumor microenvironment displays immunosuppression and nonfunctional vasculature, two key features of therapy resistance. Mechanistically, IL34 increases migration of monocyte-derived tumor-associated macrophages (MD-TAMs) in primary tumors and lung metastases through colony-stimulating factor 1 receptor (CSF1R). Blockade of CSF1R by the Food and Drug Administration-approved drug pexidartinib contrasts MD-TAMs accumulation observed in the IL34-enriched microenvironment and improves response to sunitinib or anti-PD1 treatment to reduce metastatic growth. Altogether, our data highlight the role of the IL34-CSF1R axis in regulating the tumor immune-vascular crosstalk in RCC and indicate pexidartinib as a therapeutic alternative in combination with current therapies.
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