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核因子-κB、炎症与胰腺癌发生:作为化学预防靶点的核因子-κB(综述)

NF-kappaB, inflammation and pancreatic carcinogenesis: NF-kappaB as a chemoprevention target (review).

作者信息

Zhang Zhiquan, Rigas Basil

机构信息

Department of Medicine, Division of Cancer Prevention, SUNY at Stony Brook, Stony Brook, NY 11794-5200, USA.

出版信息

Int J Oncol. 2006 Jul;29(1):185-92.

Abstract

Pancreatic cancer is the most deadly of all gastrointestinal malignancies with near zero five-year survival. This review summarizes our understanding of the potentially important role of inflammation in cancer in general and pancreatic cancer in particular. Nuclear factor kappaB (NF-kappaB), a mediator of inflammatory responses, plays a significant role in carcinogenesis and is now emerging as a link between inflammation and cancer. NF-kappaB is activated in over two thirds of human pancreatic cancers; participates in early events of pancreatic carcinogenesis through its interactions with signaling pathways; and suppression of its activation restores pancreatic cell kinetics, mainly normalizing the suppressed apoptosis of pancreatic cancer. NF-kappaB is an excellent target for chemoprevention and its modulation for pancreatic cancer prevention appears promising. The next few years will likely expand our understanding of NF-kappaB biology; solidify NF-kappaB's role as a major link between chronic inflammation and pancreatic carcinogenesis; and witness the development of NF-kappaB-based approaches to pancreatic cancer prevention.

摘要

胰腺癌是所有胃肠道恶性肿瘤中致死率最高的,其五年生存率几乎为零。本综述总结了我们对炎症在一般癌症尤其是胰腺癌中潜在重要作用的理解。核因子κB(NF-κB)作为炎症反应的介质,在致癌过程中发挥着重要作用,目前正成为炎症与癌症之间的一个联系环节。NF-κB在超过三分之二的人类胰腺癌中被激活;通过与信号通路相互作用参与胰腺癌发生的早期事件;抑制其激活可恢复胰腺细胞动力学,主要是使胰腺癌中被抑制的细胞凋亡正常化。NF-κB是化学预防的一个极佳靶点,对其进行调节以预防胰腺癌似乎很有前景。未来几年可能会扩展我们对NF-κB生物学的理解;巩固NF-κB作为慢性炎症与胰腺癌发生之间主要联系的作用;并见证基于NF-κB的胰腺癌预防方法的发展。

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