Murine Models of Gastric Corpus Preneoplasia.
Murine Models of Gastric Corpus Preneoplasia.
复制标题
胃血管质体的鼠模型。
DOI：
10.1016/j.jcmgh.2016.11.001
复制
发表时间：
2017-01
影响因子：
7.2
通讯作者：
Goldenring JR
中科院分区：
文献类型：
--
作者：
Petersen CP;Mills JC;Goldenring JR
肠型胃腺癌是在已有化生的基础上发展而来的。在过去的20年中，已经开发了许多小鼠模型来解决化生诱导的生理学和病理生理学方面的问题。虽然这些模型都没有实现真正的重演腺癌的诱导，他们导致了重要的见解的因素，影响化生的诱导和进展。在这里，我们回顾了相关的病理学定义的改变，胃体谱系和分类化生的特定谱系标志物。此外，我们回顾了目前的小鼠模型的诱导和进展的痉挛多肽（TFF2）表达化生，主要化生谱系中观察到的小鼠模型。这些模型为更广泛地了解胃化生的生理和病理生理作用提供了基础。
Intestinal-type gastric adenocarcinoma evolves in a field of pre-existing metaplasia. Over the past 20 years, a number of murine models have been developed to address aspects of the physiology and pathophysiology of metaplasia induction. Although none of these models has achieved true recapitulation of the induction of adenocarcinoma, they have led to important insights into the factors that influence the induction and progression of metaplasia. Here, we review the pathologic definitions relevant to alterations in gastric corpus lineages and classification of metaplasia by specific lineage markers. In addition, we review present murine models of the induction and progression of spasmolytic polypeptide (TFF2)–expressing metaplasia, the predominant metaplastic lineage observed in murine models. These models provide a basis for the development of a broader understanding of the physiological and pathophysiological roles of metaplasia in the stomach.