...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Mutation Research: International Journal on Mutagenesis, Chromosome Breakage and Related Subjects >Mechanisms of intestinal inflammation and development of associated cancers: lessons learned from mouse models.
【24h】

Mechanisms of intestinal inflammation and development of associated cancers: lessons learned from mouse models.

机译：肠道炎症机制和相关癌症的发展：从小鼠模型中学到的经验。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chronic inflammation is strongly associated with approximately 1/5th of all human cancers. Arising from combinations of factors such as environmental exposures, diet, inherited gene polymorphisms, infections, or from dysfunctions of the immune response, chronic inflammation begins as an attempt of the body to remove injurious stimuli; however, over time, this results in continuous tissue destruction and promotion and maintenance of carcinogenesis. Here we focus on intestinal inflammation and its associated cancers, a group of diseases on the rise and affecting millions of people worldwide. Intestinal inflammation can be widely grouped into inflammatory bowel diseases (ulcerative colitis and Crohn's disease) and celiac disease. Long-standing intestinal inflammation is associated with colorectal cancer and small-bowel adenocarcinoma, as well as extraintestinal manifestations, including lymphomas and autoimmune diseases. This article highlights potential mechanisms of pathogenesis in inflammatory bowel diseases and celiac disease, as well as those involved in the progression to associated cancers, most of which have been identified from studies utilizing mouse models of intestinal inflammation. Mouse models of intestinal inflammation can be widely grouped into chemically induced models; genetic models, which make up the bulk of the studied models; adoptive transfer models; and spontaneous models. Studies in these models have lead to the understanding that persistent antigen exposure in the intestinal lumen, in combination with loss of epithelial barrier function, and dysfunction and dysregulation of the innate and adaptive immune responses lead to chronic intestinal inflammation. Transcriptional changes in this environment leading to cell survival, hyperplasia, promotion of angiogenesis, persistent DNA damage, or insufficient repair of DNA damage due to an excess of proinflammatory mediators are then thought to lead to sustained malignant transformation. With regards to extraintestinal manifestations such as lymphoma, however, more suitable models are required to further investigate the complex and heterogeneous mechanisms that may be at play.
机译：慢性炎症与所有人类癌症的约1/5密切相关。由于环境暴露，饮食，遗传基因多态性，感染或免疫应答功能障碍等多种因素的综合作用，慢性炎症开始于人体消除有害刺激的尝试。然而，随着时间的流逝，这导致连续的组织破坏以及促进和维持癌变。在这里，我们关注肠道炎症及其相关的癌症，这是一种正在上升并影响着全球数百万人的疾病。肠道炎症可分为炎症性肠病（溃疡性结肠炎和克罗恩病）和乳糜泻。长期存在的肠道炎症与大肠癌，小肠腺癌以及肠外表现（包括淋巴瘤和自身免疫性疾病）有关。本文重点介绍了炎症性肠病和腹腔疾病以及与癌症发展相关的潜在发病机理，其中大多数已从利用小鼠肠道炎症模型进行的研究中确定。肠道炎症的小鼠模型可以广泛归类为化学诱导的模型。遗传模型，构成了所研究模型的大部分;过继转移模型;和自发模型。在这些模型中的研究已经导致人们理解，肠道内持续的抗原暴露与上皮屏障功能的丧失以及先天和适应性免疫反应的功能障碍和失调会导致慢性肠道炎症。然后认为在这种环境中的转录变化会导致细胞存活，增生，促进血管生成，持续的DNA损伤或由于过量的促炎性介质而导致的DNA损伤修复不足，从而导致持续的恶性转化。关于肠外表现，例如淋巴瘤，需要更合适的模型来进一步研究可能发挥作用的复杂和异质机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号