ArticleDiscover oncology2025
Nicotine and tar-multiple targets synergize to alter the immune micro-environment to induce prostate cancer.
Article in Discover oncology, 2025. 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
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.
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.
- Plasma-Derived sEVs from HNSCC Patients Differentially Regulate NF-κB Signaling in Macrophages Depending on the HPV Status.Cancers · 2026Article
- Advances in the immunological microenvironment and immunotherapy of bladder cancer.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProstate cancer (PC) is a common urinary system malignancy in men, and smoking is a clear risk factor. Among them, nicotine and tar in cigarettes play a key role in the development of PC, but the specific mechanism is not completely clear.
objectiveTo explore the mechanism of PC immune inflammation caused by nicotine and tar, and to provide the theoretical basis and new targets for the prevention and treatment of PC.
methodsThrough network toxicology and immune infiltration analysis, to analyze the effects of nicotine and tar on PC related cells and tissues, and machine analysis of related cytokines, signaling pathway and gene expression changes. Key genes were validated by immunohistochemistry and in vitro cellular assays.
resultsThis study screened multiple targets of nicotine and tar that may be related to the occurrence of PC. In addition, based on these targets and signaling pathways, they may be key molecular mechanisms leading to PC. In the formation and progression of PC, we found significant infiltration of M2 macrophages, with increased secretion of VEGF, MMPs, IL-10, etc., promoting tumor angiogenesis, extracellular matrix degradation, and leading to immune escape in the body. Inhibition of T cell activity, macrophages interact with tumor cells, smooth muscle cells, affect each other's functions. Functional of CD8 + T cells, tumor cells promote immune escape by binding of PD-L1 and PD-1. Hub targets such as MAOA and MAOB are affected by nicotine and tar, interference with neurotransmitters, hormones, lipid metabolism, activation of the inflammatory signals, altering the immune microenvironment, to promote the development and development of PC.
conclusionNicotine and tar may contribute to the development of PC through complex immuno-inflammatory mechanisms, and in-depth study of these mechanisms could help develop more effective prevention and treatment strategies for PC.
Indexed as
Identifiers
What Socratic 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 Socratic graph.