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Updated: Feb 11, 2026

Generation of Prostate Cancer Patient Derived Xenograft Models from Circulating Tumor Cells
Published on: October 20, 2015
Smoking Behavior Is Associated With an Altered Immune Landscape in Prostate Cancer: Implications for Patient
Amod Sharma1,2, Sarabjeet Kour Sudan1,2, Mohammad Aslam Khan3
1Department of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Active smoking promotes an immunosuppressive tumor microenvironment (TME) in prostate cancer (PCa), increasing regulatory T cells and tumor-associated macrophages. Smoking cessation may reverse these immune changes, improving PCa patient outcomes.
Area of Science:
- Oncology
- Immunology
- Cancer Research
Background:
- Smoking is a known risk factor for prostate cancer (PCa) diagnosis, recurrence, and mortality.
- The impact of smoking on the tumor microenvironment (TME) immune landscape in PCa is not well understood.
- This study explores how smoking alters the PCa immune profile and its correlation with patient survival.
Purpose of the Study:
- To investigate the effect of smoking on the immune cell composition within the PCa TME.
- To identify specific immune pathways and gene expression changes associated with smoking in PCa.
- To determine the association between smoking-induced immune alterations and PCa patient survival.
Main Methods:
- Multiplex gene expression analysis of immune cells in tumor tissues from smokers and nonsmokers using the nanoString nCounter® PanCancer immune profiling panel.
- Bioinformatic analysis using Enrichr to identify differentially activated pathways.
- Survey of public databases to correlate gene expression and immune cell abundance with patient survival data.
Main Results:
- Current smokers showed significantly higher infiltration of tumor-associated macrophages (TAMs) and regulatory T cells (Tregs) compared to nonsmokers.
- A strong positive correlation between TAMs and Tregs was observed, particularly in current smokers.
- Upregulation of immunosuppressive pathways (e.g., PD-L1 expression) and downregulation of antigen-presentation pathways were identified in smokers.
- Key upregulated genes (MAGEA3, POU2AF1, SEMG1) correlated with immune suppression and poorer survival.
- High TAM and Treg infiltration significantly correlated with reduced overall survival.
Conclusions:
- Active smoking induces an immunosuppressive TME in prostate cancer, potentially promoting tumor growth and progression.
- These smoking-induced immune changes are linked to poorer patient survival outcomes.
- Smoking cessation may offer a strategy to reverse these immunosuppressive effects and improve PCa disease outcomes.
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