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幽门螺杆菌与肠型胃癌的分子发病机制。

Helicobacter pylori and the molecular pathogenesis of intestinal-type gastric carcinoma.

机构信息

Department of Environmental and Preventive Medicine, Faculty of Medicine, Oita University, Yufu, Japan.

出版信息

Expert Rev Anticancer Ther. 2014 Aug;14(8):947-54. doi: 10.1586/14737140.2014.911092. Epub 2014 May 7.

Abstract

Gastric carcinoma is an inflammation-related cancer caused by long-term infection with the human bacterial pathogen, Helicobacter pylori. The pattern of acute-on-chronic inflammation causes progressive mucosal damage which may result in atrophy with metaplastic epithelia and eventually gastric cancer. Recently, it has been recognized that H. pylori can also cause genetic instability such as double-stranded DNA breaks and can produce gene activation and silencing via epigenetic pathways. As genetic instability is the hallmark of cancer, we highlight recent progress in understanding the gastric carcinogenesis in relation to H. pylori-related inflammation, H. pylori-induced double-stranded DNA breakage and aberrant gene expression as well as the mechanisms and role of H. pylori-associated epigenetic change in gene expression.

摘要

胃癌是一种与炎症相关的癌症,由长期感染人类细菌病原体幽门螺杆菌引起。急慢性炎症的模式导致进行性的黏膜损伤,可能导致萎缩伴上皮化生,最终发展为胃癌。最近,人们已经认识到幽门螺杆菌还可以引起遗传不稳定性,如双链 DNA 断裂,并可以通过表观遗传途径产生基因激活和沉默。由于遗传不稳定性是癌症的标志,我们重点介绍了近年来在理解与幽门螺杆菌相关炎症、幽门螺杆菌诱导的双链 DNA 断裂和异常基因表达以及幽门螺杆菌相关表观遗传变化在基因表达中的机制和作用相关的胃癌发生机制方面的最新进展。

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