2007 April ; 7(4): 256–269. doi:10.1038/nrc2090. | Angelo M. De Marzo†‡, Elizabeth A. Platz§, Siobhan Sutcliffe§, Jianfeng Xu†, Henrik Grönberg†, Charles G. Drake†, Yasutomo Nakai#, William B. Isaacs**, and William G. Nelson†
The article reviews the role of inflammation in prostate carcinogenesis, proposing that chronic inflammatory states, often triggered by environmental factors such as infectious agents and dietary carcinogens, lead to the development of proliferative inflammatory atrophy (PIA) and subsequent prostate cancer. The authors discuss the evidence from epidemiological, histopathological, and molecular pathological studies, highlighting the importance of understanding the mechanisms of inflammation in prostate cancer development. They also explore potential sources of prostatic inflammation, including infectious agents, urine reflux, dietary factors, and oestrogens. The article further examines the immunobiology of prostate inflammation, focusing on the role of various inflammatory cells and genes involved in innate and acquired immunity. Finally, the authors propose a 'injury and regeneration' hypothesis to explain the progression from inflammation to cancer and suggest future research directions to better understand and potentially prevent prostate cancer.The article reviews the role of inflammation in prostate carcinogenesis, proposing that chronic inflammatory states, often triggered by environmental factors such as infectious agents and dietary carcinogens, lead to the development of proliferative inflammatory atrophy (PIA) and subsequent prostate cancer. The authors discuss the evidence from epidemiological, histopathological, and molecular pathological studies, highlighting the importance of understanding the mechanisms of inflammation in prostate cancer development. They also explore potential sources of prostatic inflammation, including infectious agents, urine reflux, dietary factors, and oestrogens. The article further examines the immunobiology of prostate inflammation, focusing on the role of various inflammatory cells and genes involved in innate and acquired immunity. Finally, the authors propose a 'injury and regeneration' hypothesis to explain the progression from inflammation to cancer and suggest future research directions to better understand and potentially prevent prostate cancer.