ArticleCells2025
Immunosuppression of Tumor-Derived Factors Modulated Neutrophils in Upper Tract Urothelial Carcinoma Through Upregulation of Arginase-1 via ApoA1-STAT3 Axis.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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Who cites it
4 citing papers in PubMed.
- Intersecting Roles of Estrogens and Neutrophils in Modulating Innate Immunity in Cancer.Biomolecules · 2026Review
- Tumor derived adiponectin induces immunosuppressive macrophages in upper tract urothelial carcinoma.Translational oncology · 2026Article
- Metabolic Control of Immunity-Unveiling Neutrophil Mechanisms.Advances in experimental medicine and biology · 2026Review
- Neutrophil-to-apolipoprotein A1 ratio as a novel biomarker for prognosis in anti-NMDAR encephalitis: a retrospective cohort analysis.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Upper tract urothelial carcinoma (UTUC) presents aggressive features and a tumor microenvironment with T cell depletion. However, the role of tumor-associated neutrophils in UTUC remains unclear. This study aimed to investigate how UTUC tumor-derived factors modulate neutrophils and their impact on T cell immune responses. Our findings demonstrate that UTUC secreted tumor-derived factors, with apolipoprotein A1 (Apo-A1) being the predominant factor, which upregulated arginase-1 expression in neutrophils. STAT3 activation was responsible for the upregulation of arginase-1 in neutrophils. Blocking the interactions between Apo-A1 and its receptors reduced arginase-1 expression in neutrophils treated with tumor tissue culture supernatant (TTCS). Moreover, both CD4
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Registered trials
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