Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Jan;60(1):199-215.
doi: 10.1111/j.1365-2559.2011.04033.x.

Prostate cancer and inflammation: the evidence

Affiliations
Review

Prostate cancer and inflammation: the evidence

Karen S Sfanos et al. Histopathology. 2012 Jan.

Abstract

Chronic inflammation is now known to contribute to several forms of human cancer, with an estimated 20% of adult cancers attributable to chronic inflammatory conditions caused by infectious agents, chronic non-infectious inflammatory diseases and/or other environmental factors. Indeed, chronic inflammation is now regarded as an 'enabling characteristic' of human cancer. The aim of this review is to summarize the current literature on the evidence for a role for chronic inflammation in prostate cancer aetiology, with a specific focus on recent advances regarding the following: (i) potential stimuli for prostatic inflammation; (ii) prostate cancer immunobiology; (iii) inflammatory pathways and cytokines in prostate cancer risk and development; (iv) proliferative inflammatory atrophy (PIA) as a risk factor lesion to prostate cancer development; and (v) the role of nutritional or other anti-inflammatory compounds in reducing prostate cancer risk.

PubMed Disclaimer

Figures

Figure 1
Figure 1
(A), Example of prostatic corpora amylacea. Note physical trauma to glandular epithelium (arrow) and associated surrounding focal chronic inflammation (arrowheads). Immunohistochemistry (IHC) for lactoferrin (B) and calprotectin (C) on prostate tissue sections containing corpora amylacea.
Figure 2
Figure 2
Example of proliferative inflammatory atrophy (PIA) lesion. A, Haematoxylin and eosin (H&E) and B, immunohistochemistry (IHC) for Ki-67 proliferation marker shows relatively high fraction of luminal epithelial cells staining (compared to normal appearing epithelium which is not shown).
Figure 3
Figure 3. Example of post-atrophic hyperplasia (PAH), a form of PIA
A, Haematoxylin and eosin (H&E) arrows point to PAH, which shows mild stromal inflammation. Arrowheads point to carcinoma. B, Immunohistochemistry (IHC) for Ki-67. C, IHC for ‘basal specific’ cytokeratin (CK903). Note that, as is characteristic of most forms of prostatic atrophy, many cells in the luminal cell layer stain positive with this antibody as well as other antibodies against keratin 5.

References

    1. Siegel R, Ward E, Brawley O, Jemal A. Cancer statistics, 2011. CA Cancer J Clin. 2011;61:212–236. - PubMed
    1. De Marzo AM, Platz EA, Sutcliffe S, et al. Inflammation in prostate carcinogenesis. Nat Rev Cancer. 2007;7:256–269. - PMC - PubMed
    1. Krieger JN, Nyberg L, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA. 1999;282:236–237. - PubMed
    1. Brede CM, Shoskes DA. The etiology and management of acute prostatitis. Nat Rev Urol. 2011;8:207–212. - PubMed
    1. Cai T, Mazzoli S, Meacci F, et al. Epidemiological features and resistance pattern in uropathogens isolated from chronic bacterial prostatitis. J Microbiol. 2011;49:448–454. - PubMed