ArticleJournal of applied toxicology : JAT2026
Immunomodulation of the Prostate Tumor Microenvironment Following Inorganic Arsenic Exposure.
Article in Journal of applied toxicology : JAT, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Immune remodeling in chronic prostatitis: from microenvironment imbalance to targeted therapy.Frontiers in molecular biosciences · 2026Article
- Editorial: New insights in veterinary cancer immunology, volume II.Frontiers in veterinary science · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The tumor microenvironment (TME) influences prostate cancer (PCa) progression through stromal and immune interactions. Adipose-derived mesenchymal stromal cells (ASCs) modulate immune tone, while inorganic arsenic (iAs), a widespread toxicant, is linked to immune suppression and carcinogenesis. Their combined impact on PCa immunity has remained unclear. Using a Ras-driven murine PCa model (TC2Ras, which mimics aggressive, immune-interactive PCa through constitutive Ras signaling), we assessed ASC and chronic iAs exposure effects on tumor growth, immune infiltration, and transcriptomic remodeling via flow cytometry, RNA-seq, and qPCR. ASC-conditioned media increased TC2Ras viability by up to 82%, an effect reversed by iAs (300-1000 ppb). In vivo, ASC co-implantation significantly elevated tumor weight in ASC + iAs tumors. ASC promoted approximately twofold macrophage and CD4
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