Okada Futoshi
Division of Pathological Biochemistry, Department of Biomedical Sciences, School of Life Science, Tottori University Faculty of Medicine, Yonago 683-8503, Japan ; †Chromosome Engineering Research Center, Tottori University, Yonago 683-8503, Japan.
Yonago Acta Med. 2014 Jun;57(2):65-72. Epub 2014 Jul 30.
Inflammation is a definite cancer-causing factor as revealed by cumulative basic, clinical and epidemiological studies. It is mostly induced by infectious agents. For instance, infection with papillomaviruses associates with anogenital cancers, especially cervical cancers; Helicobacter pylori infection of the stomach tends to increase the risk of stomach cancer; chronic hepatitis B & C viruses and fluke infections of the liver increase liver cancers; autoimmune diseases, e.g., inflammatory bowel diseases, associate with development of colorectal cancer, and aerial irritants (foreign bodies) such as asbestos or fine particulate matter (PM2.5) in outdoor air increase malignant pleural mesotheliomas or lung cancers. These are typical examples of inflammation-related carcinogenesis. It is apparent that the pathogens to induce inflammatory reactions in specific organs are not related to each other. However, the underlying pathogenesis in common is to induce and/or sustain inflammation. In this article, I would like to review the up-to-date findings of epidemiological trends, causes and mechanisms of inflammation-related carcinogenesis.
累积的基础、临床和流行病学研究表明，炎症是一种确切的致癌因素。它大多由感染因子诱发。例如，乳头瘤病毒感染与肛门生殖器癌症，尤其是宫颈癌相关；胃部幽门螺杆菌感染往往会增加患胃癌的风险；慢性乙型和丙型肝炎病毒以及肝脏的吸虫感染会增加肝癌的发生几率；自身免疫性疾病，如炎症性肠病，与结直肠癌的发生有关，而空气中的刺激物（异物），如户外空气中的石棉或细颗粒物（PM2.5）会增加恶性胸膜间皮瘤或肺癌的发生风险。这些都是炎症相关致癌作用的典型例子。显然，在特定器官中诱发炎症反应的病原体彼此之间并无关联。然而，共同的潜在发病机制是诱发和/或维持炎症。在本文中，我将回顾炎症相关致癌作用的流行病学趋势、病因及机制的最新研究结果。
