The Role of Inflammation in Pancreatic Cancer

被引：87

作者：

Hausmann, Simone ^{[1
]}

Kong, Bo ^{[1
]}

Michalski, Christoph ^{[1
]}

Erkan, Mert ^{[1
]}

Friess, Helmut ^{[1
]}

机构：

[1] Tech Univ Munich, Dept Surg, Klinikum Rechts Isar, D-81675 Munich, Germany

来源：

INFLAMMATION AND CANCER | 2014年 / 816卷

关键词：

NF-KAPPA-B; UROKINASE PLASMINOGEN-ACTIVATOR; BETA SIGNALING PATHWAYS; EPIDERMAL-GROWTH-FACTOR; PHASE-II TRIAL; DUCTAL ADENOCARCINOMA; ENHANCED EXPRESSION; CELL-LINES; MATRIX METALLOPROTEINASE-2; INTRAEPITHELIAL NEOPLASIA;

D O I：

10.1007/978-3-0348-0837-8_6

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with an extremely poor prognosis. Inflammatory processes have emerged as key mediators of pancreatic cancer development and progression. In genetically engineered mouse models, induction of pancreatitis accelerates PDAC development, and patients with chronic pancreatitis are known to have a higher risk of developing pancreatic cancer. In recent years, much effort has been given to identify the underlying mechanisms that contribute to inflammation-induced tumorigenesis. Many inflammatory pathways have been identified and inhibitors have been developed in order to prevent cancer development and progression. In this chapter, we discuss the role of inflammatory pathways in the initiation and progression of pancreatic cancer as well as the role of inhibitors used in treatment and prevention of pancreatic cancer.

引用

页码：129 / 151

页数：23

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