Martin Puhr1, Angelo De Marzo2, William Isaacs3, Marshall Scott Lucia4, Karen Sfanos2, Srinivasan Yegnasubramanian5, Zoran Culig6. 1. Experimental Urology, Department of Urology, Medical University of Innsbruck, Innsbruck, Austria. 2. Department of Pathology, Sidney Kimmel Comprehensive Cancer Center, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Urology, Sidney Kimmel Comprehensive Cancer Center, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 3. Department of Urology, Sidney Kimmel Comprehensive Cancer Center, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 4. Department of Pathology, Sidney Kimmel Comprehensive Cancer Center, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 5. Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 6. Experimental Urology, Department of Urology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: zoran.culig@i-med.ac.at.
Abstract
CONTEXT: Chronic inflammation of the prostate has been associated with preneoplastic lesions and cancer development. Multiple causes have been considered for chronic inflammation of the prostate. Inflammatory cytokines such as interleukins are implicated in prostate carcinogenesis and development. OBJECTIVE: To evaluate literature published on etiological factors, urinary microbiota, morphological features of proliferative inflammatory atrophy and high-grade prostate intraepithelial neoplasia, genetic polymorphisms, inflammatory stress, and cytokine signaling. EVIDENCE ACQUISITION: We searched literature from PubMed from 2010 and also included the most important publications from the previous period. EVIDENCE SYNTHESIS: Prostate cancer inflammation and premalignant lesions have been frequently discussed in scientific literature. A limited number of models are available for studying inflammation and premalignant lesions. However, morphological pathology could be complemented by analysis of gene polymorphisms in these patients and appropriate functional studies. CONCLUSIONS: Prostatitis could be caused by bacterial or viral infections, dietary compounds, and changes in testosterone:estradiol ratio. In some cases, the microbiota can exert direct effects on cancer development. Prostate inflammatory atrophy or high grade prostate intraepithelial neoplasia have been associated with response to cellular stress and have been discussed in connection to early cancer development. A large number of genetic polymorphisms have been identified in inflammatory prostate. Genetic and epigenetic alterations may be a consequence of the proinflammatory stress in the prostate. Proinflammatory cytokines interleukin-6 and -8 contribute to prostate malignancy; however, their function was more frequently investigated in cancer tissue rather than in inflammation. PATIENT SUMMARY: We performed a review of recent literature related to prostate inflammation, microbiota, and prostate cancer. New functional approaches are required for a better understanding of the role of inflammation and cancer development.
CONTEXT: Chronic inflammation of the prostate has been associated with preneoplastic lesions and cancer development. Multiple causes have been considered for chronic inflammation of the prostate. Inflammatory cytokines such as interleukins are implicated in prostate carcinogenesis and development. OBJECTIVE: To evaluate literature published on etiological factors, urinary microbiota, morphological features of proliferative inflammatory atrophy and high-grade prostate intraepithelial neoplasia, genetic polymorphisms, inflammatory stress, and cytokine signaling. EVIDENCE ACQUISITION: We searched literature from PubMed from 2010 and also included the most important publications from the previous period. EVIDENCE SYNTHESIS: Prostate cancer inflammation and premalignant lesions have been frequently discussed in scientific literature. A limited number of models are available for studying inflammation and premalignant lesions. However, morphological pathology could be complemented by analysis of gene polymorphisms in these patients and appropriate functional studies. CONCLUSIONS: Prostatitis could be caused by bacterial or viral infections, dietary compounds, and changes in testosterone:estradiol ratio. In some cases, the microbiota can exert direct effects on cancer development. Prostate inflammatory atrophy or high grade prostate intraepithelial neoplasia have been associated with response to cellular stress and have been discussed in connection to early cancer development. A large number of genetic polymorphisms have been identified in inflammatory prostate. Genetic and epigenetic alterations may be a consequence of the proinflammatory stress in the prostate. Proinflammatory cytokines interleukin-6 and -8 contribute to prostate malignancy; however, their function was more frequently investigated in cancer tissue rather than in inflammation. PATIENT SUMMARY: We performed a review of recent literature related to prostate inflammation, microbiota, and prostate cancer. New functional approaches are required for a better understanding of the role of inflammation and cancer development.