Critical role of NF-κB in pancreatic cancer
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Lakshmi Prabhu1, Rasika Mundade1, Murray Korc2,3, Patrick J. Loehrer4, Tao Lu1,3,5
1Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA
2Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA
3Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA
4Division of Hematology and Oncology, Indiana Cancer Pavilion, Indianapolis, IN, USA
5Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA
Tao Lu, e-mail: email@example.com
Keywords: NF-κB, pancreatic cancer
Received: August 26, 2014 Accepted: October 23, 2014 Published: December 19, 2014
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, and in spite of intense efforts there are limited therapeutic options for patients with PDAC. PDACs harbor a high frequency of Kras mutations and other driver mutations that lead to altered signaling pathways and contribute to therapeutic resistance. Importantly, constitutive activation of nuclear factor κB (NF-κB) is frequently observed in PDAC. An increasing body of evidence suggests that both classical and non-classical NF-κB pathways play a crucial role in PDAC development and progression. In this review, we update the most recent advances regarding different aspects of NF-κB involvement in PDAC development and progression, emphasizing its potential as a therapeutic target and the need to discover pathway-specific cytosolic NF-κB regulators which could be used to design novel therapeutic strategies for PDAC.
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