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核因子κB在胰腺癌中的作用及靶向治疗的临床应用

The role of nuclear factor kappaB in pancreatic cancer and the clinical applications of targeted therapy.

作者信息

Holcomb Bryan, Yip-Schneider Michele, Schmidt C Max

机构信息

Department of Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

出版信息

Pancreas. 2008 Apr;36(3):225-35. doi: 10.1097/MPA.0b013e31815b3207.

Abstract

Pancreatic cancer is one of the leading causes of cancer mortality in the United States. Current therapy for pancreatic cancer involves surgery, chemotherapy, and radiation therapy; however, the 5-year survival rate remains less than 5%. New strategies for treating pancreatic cancer include targeting intracellular signaling that provides survival advantages to cancer cells. One of these targets is the transcription factor nuclear factor (NF) kappaB, which is activated by a variety of mechanisms. Data demonstrate that increased NF-kappaB activity can promote growth and tumorigenesis, inhibit apoptosis, promote angiogenesis, promote invasion and metastasis, and promote chemoresistance in pancreatic cancer. This review explores the roles of NF-JB in these processes and examines the evidence that different NF-kappaB-inhibiting drugs can improve the treatment of pancreatic cancer.

摘要

胰腺癌是美国癌症死亡的主要原因之一。目前胰腺癌的治疗方法包括手术、化疗和放疗;然而,5年生存率仍低于5%。治疗胰腺癌的新策略包括靶向为癌细胞提供生存优势的细胞内信号传导。其中一个靶点是转录因子核因子(NF)κB,它可通过多种机制被激活。数据表明,NF-κB活性增加可促进胰腺癌的生长和肿瘤发生、抑制细胞凋亡、促进血管生成、促进侵袭和转移以及促进化疗耐药。本综述探讨了NF-κB在这些过程中的作用,并研究了不同NF-κB抑制药物可改善胰腺癌治疗的证据。

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