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幽门螺杆菌在胃癌发生中的作用机制。

Helicobacter pylori in gastric carcinogenesis: mechanisms.

机构信息

Department of Medicine, Vanderbilt University, Nashville, TN 37232, USA.

出版信息

Gastroenterol Clin North Am. 2013 Jun;42(2):285-98. doi: 10.1016/j.gtc.2013.01.006. Epub 2013 Mar 6.

DOI:10.1016/j.gtc.2013.01.006
PMID:23639641
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3648881/
Abstract

Helicobacter pylori infection induces chronic inflammation and is the strongest known risk factor for gastric cancer. The genomes of H pylori are highly diverse and therefore bacterial virulence factors play an important role in determining the outcome of H pylori infection, in combination with host responses that are augmented by environmental and dietary risk factors. It is important to gain further understanding of the pathogenesis of H pylori infection to develop more effective treatments for this common but deadly malignancy. This review focuses on the specific mechanisms used by H pylori to drive gastric carcinogenesis.

摘要

幽门螺杆菌感染会引起慢性炎症,是已知的最强胃癌风险因素。幽门螺杆菌的基因组高度多样化,因此细菌的毒力因子在确定幽门螺杆菌感染的结果方面起着重要作用,这与宿主反应相结合,宿主反应会受到环境和饮食风险因素的增强。深入了解幽门螺杆菌感染的发病机制对于开发针对这种常见但致命恶性肿瘤的更有效治疗方法非常重要。本文综述重点关注了幽门螺杆菌用于驱动胃癌发生的特定机制。

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本文引用的文献

1
Iron deficiency accelerates Helicobacter pylori-induced carcinogenesis in rodents and humans.缺铁加速了幽门螺杆菌在啮齿动物和人类中的致癌作用。
J Clin Invest. 2013 Jan;123(1):479-92. doi: 10.1172/JCI64373. Epub 2012 Dec 21.
2
Reactive oxygen species-induced autophagic degradation of Helicobacter pylori CagA is specifically suppressed in cancer stem-like cells.活性氧诱导的幽门螺杆菌 CagA 自噬降解在肿瘤干细胞样细胞中被特异性抑制。
Cell Host Microbe. 2012 Dec 13;12(6):764-77. doi: 10.1016/j.chom.2012.10.014.
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Pathogenic bacterium Helicobacter pylori alters the expression profile of p53 protein isoforms and p53 response to cellular stresses.致病细菌幽门螺杆菌改变了 p53 蛋白异构体的表达谱,并改变了 p53 对细胞应激的反应。
Proc Natl Acad Sci U S A. 2012 Sep 18;109(38):E2543-50. doi: 10.1073/pnas.1205664109. Epub 2012 Aug 27.
4
Structural insights into Helicobacter pylori oncoprotein CagA interaction with β1 integrin.幽门螺杆菌致癌蛋白 CagA 与β1 整合素相互作用的结构见解。
Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14640-5. doi: 10.1073/pnas.1206098109. Epub 2012 Aug 20.
5
Role of interleukin-32 in Helicobacter pylori-induced gastric inflammation.白细胞介素-32 在幽门螺杆菌诱导的胃炎症中的作用。
Infect Immun. 2012 Nov;80(11):3795-803. doi: 10.1128/IAI.00637-12. Epub 2012 Aug 13.
6
Tertiary structure-function analysis reveals the pathogenic signaling potentiation mechanism of Helicobacter pylori oncogenic effector CagA.三级结构-功能分析揭示了幽门螺杆菌致癌效应因子 CagA 的致病信号增强机制。
Cell Host Microbe. 2012 Jul 19;12(1):20-33. doi: 10.1016/j.chom.2012.05.010.
7
Relationship of IL-1 and TNF-α polymorphisms with Helicobacter pylori in gastric diseases in a Brazilian population.IL-1 和 TNF-α 多态性与巴西人群胃疾病中幽门螺杆菌的关系。
Braz J Med Biol Res. 2012 Sep;45(9):811-7. doi: 10.1590/s0100-879x2012007500099. Epub 2012 Jun 21.
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Analysis of Helicobacter pylori cagA promoter elements required for salt-induced upregulation of CagA expression.分析盐诱导上调 CagA 表达所需的幽门螺杆菌 cagA 启动子元件。
Infect Immun. 2012 Sep;80(9):3094-106. doi: 10.1128/IAI.00232-12. Epub 2012 Jun 18.
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c-Src and c-Abl kinases control hierarchic phosphorylation and function of the CagA effector protein in Western and East Asian Helicobacter pylori strains.c-Src 和 c-Abl 激酶控制西方和东亚幽门螺杆菌菌株中 CagA 效应蛋白的层次磷酸化和功能。
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The number of Helicobacter pylori CagA EPIYA C tyrosine phosphorylation motifs influences the pattern of gastritis and the development of gastric carcinoma.幽门螺杆菌 CagA EPIYA C 酪氨酸磷酸化基序的数量影响胃炎的模式和胃癌的发展。
Histopathology. 2012 May;60(6):992-8. doi: 10.1111/j.1365-2559.2012.04190.x. Epub 2012 Feb 20.