炎症、萎缩与前列腺癌发生

Inflammation, atrophy, and prostate carcinogenesis.

作者信息

De Marzo Angelo M, Nakai Yasutomo, Nelson William G

机构信息

Department of Pathology, Johns Hopkins University, Baltimore, MD 21231, USA.

出版信息

Urol Oncol. 2007 Sep-Oct;25(5):398-400. doi: 10.1016/j.urolonc.2007.05.007.

DOI:10.1016/j.urolonc.2007.05.007

PMID:17826659

Abstract

The etiological agents that cause prostate cancer remain unknown. There is emerging evidence that "risk factor" lesions that are proposed to represent regenerative epithelium in response to environmental insults may precede the development of prostatic intraepithelial neoplasia and early carcinoma. Recent evidence suggests that these lesions, referred to collectively as proliferative inflammatory atrophy, may arise in the setting of inflammation and dietary toxins, such as "charred meat" carcinogens. Additional epidemiological, molecular pathological, and animal model work needs to be done to determine whether inflammation and atrophy are "driving" prostate carcinogenesis.

摘要

导致前列腺癌的病原体仍然未知。越来越多的证据表明，被认为是对环境损伤作出反应的再生上皮的“风险因素”病变，可能先于前列腺上皮内瘤变和早期癌的发生。最近的证据表明，这些病变统称为增殖性炎性萎缩，可能在炎症和饮食毒素（如“烧焦肉类”致癌物）的环境中出现。需要开展更多的流行病学、分子病理学和动物模型研究，以确定炎症和萎缩是否在“推动”前列腺癌的发生。