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首页> 外文期刊>Current opinion in gastroenterology >Cancer in inflammatory bowel disease: Lessons from animal models
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Cancer in inflammatory bowel disease: Lessons from animal models

机译：炎症性肠病的癌症：动物模型的课程

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Purpose of review: Human colitis-associated cancers (CAC) represent a heterogeneous group of conditions in which multiple oncogenic pathways are involved. In this article, we review the latest studies using genetic, chemical, bacterial and innate immune-mediated experimental models of CAC. Recent findings: Using the azoxymethane-dextran sodium sulfate model, wound healing pathways seem to be required in the development of CAC. There is also an emerging understanding that commensal and/or pathogenic bacteria can promote tumorigenesis, through T cell and TLR-mediated inflammation. Using specific transgenic mice (villin-CD98, T cell SMAD7, villin-TLR4) or specific knockout mice, investigators have determined that derangements in epithelial or innate and adaptive immune pathways can result in CAC. Subtle perturbations in epithelial repair - both too little or too exuberant - can render mice susceptible to tumorigenesis. Summary: With the aid of animal models, we have witnessed a rapid expansion of our knowledge of the molecular and immunologic mechanisms underlying inflammatory cancers. Though animal models have contributed a discrete amount of information to our understanding of tumorigenesis in the setting of intestinal inflammation, it is clear that no single animal model will be able to adequately recapitulate the pathogenesis of complex colorectal cancers, but each model gets us one step closer to comprehending the nature of CAC.
机译：审查目的：人性结肠炎相关的癌症（CAC）代表涉及多种致癌途径的异质条件组。在本文中，我们使用CAC的遗传，化学，细菌和先天免疫介导的实验模型来审查最新研究。最近的发现：使用含氮氧基甲烷 - 葡聚糖硫酸钠模型，CAC发育中伤口愈合途径似乎是所需的。还有一种新兴的理解，共生和/或致病细菌可以通过T细胞和TLR介导的炎症促进肿瘤发生。使用特定的转基因小鼠（Villin-CD98，T Cell Smad7，Villin-TLR4）或特异性敲除小鼠，研究人员已经确定了上皮或先天和自然和自适应免疫途径中的紊乱可以导致CAC。上皮修复中的微妙扰动 - 既太少或过于旺盛，都可以使小鼠易受肿瘤发生的影响。总结：借助动物模型，我们目睹了我们对炎症癌症潜在的分子和免疫机制的知识的快速扩张。虽然动物模型在肠炎症中造成了对肿瘤发生的理解的离散量的信息，但很明显，没有单一动物模型能够充分延长复杂结肠直肠癌的发病机制，但每个模型都让我们一步更接近理解CAC的性质。

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