Mueller Anne, Falkow Stanley, Amieva Manuel R
Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305-5124, USA.
Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):1859-64. doi: 10.1158/1055-9965.EPI-04-0820.
The development of gastric adenocarcinoma is closely linked to chronic infection with the bacterial pathogen Helicobacter pylori. One Helicobacter-specific virulence factor in particular, the CagA protein, has emerged as a main effector molecule in the interaction of H. pylori with gastric epithelial cells and has been implicated in gastric carcinogenesis. This review highlights the latest insights that have been gained into the pathogenesis of the disease by transcriptional profiling approaches studying gene expression in normal gastric tissue and gastric cancer tissue from human biopsy material as well as animal models of Helicobacter infection. The potential role of CagA as a bacterial oncoprotein is also discussed.
胃腺癌的发展与细菌病原体幽门螺杆菌的慢性感染密切相关。特别是一种幽门螺杆菌特异性毒力因子,即CagA蛋白,已成为幽门螺杆菌与胃上皮细胞相互作用中的主要效应分子,并与胃癌发生有关。本综述重点介绍了通过转录谱分析方法所获得的关于该疾病发病机制的最新见解,这些方法研究了来自人类活检材料的正常胃组织和胃癌组织以及幽门螺杆菌感染动物模型中的基因表达。还讨论了CagA作为细菌癌蛋白的潜在作用。