Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Methods Cell Biol. 2020;159:23-46. doi: 10.1016/bs.mcb.2020.04.011. Epub 2020 Jun 5.
While the incidence of gastric cancer in the United States is relatively low due to the diagnosis and treatment of the major risk factor Helicobacter pylori (H. pylori), 5-year patient survival is only approximately 29%. Even after H. pylori infection has been eradicated there is still a risk of developing gastric cancer. Gastric cancer is the final clinical outcome that is often initiated by a sustained inflammatory response and altered epithelial cell differentiation and metaplasia in response to H. pylori infection. Identifying the early epithelial responses to H. pylori infection is important in advancing our understanding of the events that shape a conducive environment for the progression of gastric cancer. Thus, we developed a human gastric tissue-derived organoid-based approach to identify the initiating molecular events that trigger gastric cancer development in response to bacterial infection.
虽然由于幽门螺杆菌（H. pylori）这一主要危险因素的诊断和治疗，美国胃癌的发病率相对较低，但 5 年患者生存率仅约为 29%。即使 H. pylori 感染被根除，仍有发生胃癌的风险。胃癌是一种最终的临床结果，通常是由对 H. pylori 感染的持续炎症反应以及上皮细胞分化和化生的改变引发的。鉴定对 H. pylori 感染的早期上皮反应对于加深我们对形成有利于胃癌进展的环境的事件的理解很重要。因此，我们开发了一种基于人胃组织衍生类器官的方法来鉴定细菌感染引发胃癌发展的起始分子事件。
