Abstract

About 20% of all human cancers are caused by chronic infection or chronic inflammatory states. Recently, a new hypothesis has been proposed for prostate carcinogenesis. It proposes that exposure to environmental factors such as infectious agents and dietary carcinogens, and hormonal imbalances lead to injury of the prostate and to the development of chronic inflammation and regenerative 'risk factor' lesions, referred to as proliferative inflammatory atrophy (PIA). By developing new experimental animal models coupled with classical epidemiological studies, genetic epidemiological studies and molecular pathological approaches, we should be able to determine whether prostate cancer is driven by inflammation, and if so, to develop new strategies to prevent the disease.

Author affiliations

1. Johns Hopkins University School of Medicine, Department of Pathology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins CRB-1, 1650 Orleans Street, Baltimore, MD 21231, USA.
2. Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins CRB-1, 1650 Orleans Street, Baltimore, MD 21231, USA.
3. Department of Epidemiology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA.
4. Center for Human Genomics Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
5. Karolinska Institutet Department of Medical Epidemiology and Biostatistics P.O. Box 281, SE-171 77 Stockholm, Sweden.
6. Osaka University Graduate Medicine of Urology, 2-2 Yamadaoka, Osaka 565, Japan.
7. The Brady Urological Research Institute, Department of Urology, The Johns Hopkins Hosptital, Baltimore, MD 21287, USA.

Correspondence to: Angelo M. De Marzo^1,2 Email: ademarz@jhmi.edu

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