Inflammatory bowel disease: a model of chronic inflammation-induced cancer.
Inflammatory bowel disease: a model of chronic inflammation-induced cancer.
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DOI：
10.1007/978-1-59745-447-6_9
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发表时间：
2009
影响因子：
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通讯作者：
Guang-Yu Yang;Sofia Taboada;J. Liao
中科院分区：
文献类型：
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作者：
Guang-Yu Yang;Sofia Taboada;J. Liao
慢性炎症是人类癌症发展的公认危险因素。炎症性肠病（IBD），包括溃疡性结肠炎和克罗恩病，是一种典型的长期存在的结肠炎性疾病，具有发生结直肠癌的风险增加。参与慢性炎症过程的几种分子事件可能有助于人类癌症发展的多阶段进展，包括活性氧和氮物质的过度产生，关键花生四烯酸代谢产物和细胞因子/生长因子的过度产生/活化，以及免疫系统功能障碍。已经建立了多种IBD动物模型，一般而言，这些模型可主要分为化学诱导、基因工程（转基因或基因敲除）、自发和过继转移动物模型。本章主要集中在（1）IBD与结直肠癌风险的流行病学和分子证据，（2）IBD致癌的分子发病机制，（3）IBD诱导的啮齿动物致癌模型及其应用。
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.