De Marzo Angelo M, Platz Elizabeth A, Sutcliffe Siobhan, Xu Jianfeng, Grönberg Henrik, Drake Charles G, Nakai Yasutomo, Isaacs William B, Nelson William G
Johns Hopkins University School of Medicine, Department of Pathology, Baltimore, MD, USA.
Nat Rev Cancer. 2007 Apr;7(4):256-69. doi: 10.1038/nrc2090.
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.
约20%的人类癌症是由慢性感染或慢性炎症状态引起的。最近,有人提出了一种关于前列腺癌发生的新假说。该假说认为,接触传染性病原体和膳食致癌物等环境因素以及激素失衡会导致前列腺损伤,并引发慢性炎症和再生性“危险因素”病变,即增殖性炎性萎缩(PIA)。通过开发新的实验动物模型,结合经典流行病学研究、遗传流行病学研究和分子病理学方法,我们应该能够确定前列腺癌是否由炎症驱动,如果是,进而制定预防该疾病的新策略。