Yang Guang-Yu, Taboada Sofia, Liao Jie
Department of Pathology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
Methods Mol Biol. 2009;511:193-233. doi: 10.1007/978-1-59745-447-6_9.
Chronic inflammation is a well-recognized risk factor for the development of human cancer. Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a typical longstanding inflammatory disease of the colon with increased risk for the development of colorectal carcinoma. Several molecular events involved in chronic inflammatory process may contribute to multistage progression of human cancer development, including the overproduction of reactive oxygen and nitrogen species, overproduction/activation of key arachidonic acid metabolites and cytokines/growth factors, and immunity system dysfunction. Multiple animal models of IBD have been established, and in general, these models can be mainly categorized into chemically induced, genetically engineered (transgenic or gene knock-out), spontaneous, and adoptive transferring animal models. This chapter mainly focuses on (1) epidemiologic and molecular evidence on IBD and risk of colorectal cancer, (2) molecular pathogenesis of IBD-induced carcinogenesis, and (3) modeling of IBD-induced carcinogenesis in rodents and its application.
慢性炎症是公认的人类癌症发生的风险因素。炎症性肠病（IBD），包括溃疡性结肠炎和克罗恩病，是结肠典型的长期炎症性疾病，患结直肠癌的风险增加。慢性炎症过程中涉及的几个分子事件可能导致人类癌症发生的多阶段进展，包括活性氧和氮物种的过量产生、关键花生四烯酸代谢产物和细胞因子/生长因子的过量产生/激活以及免疫系统功能障碍。已经建立了多种IBD动物模型，一般来说，这些模型主要可分为化学诱导、基因工程（转基因或基因敲除）、自发和过继转移动物模型。本章主要关注：（1）IBD与结直肠癌风险的流行病学和分子证据；（2）IBD诱导致癌的分子发病机制；（3）啮齿动物中IBD诱导致癌的建模及其应用。
