University of Pittsburgh School of Medicine, Division of Gastroenterology, Hepatology and Nutrition, Medical Arts Building, 4th floor, Office 400.5, 3708 5th Ave., Pittsburgh, PA 15213, United States.
Curr Opin Pharmacol. 2009 Aug;9(4):411-8. doi: 10.1016/j.coph.2009.06.011. Epub 2009 Jul 7.
There is a growing awareness that inflammation plays a contributory role in numerous pathologies, including pancreatic carcinogenesis. Inflammatory states are characterized by the creation of reactive oxygen species and the induction of cell cycling for tissue growth and repair. The initiation, promotion and expansion of tumors may be influenced by numerous components that function in the inflammatory response. Recognized risk factors for pancreatic cancer include cigarette smoking, chronic/hereditary pancreatitis, obesity and type II diabetes. Each risk factor is linked by the fact that the inflammatory state significantly drives its pathology. This article will outline how inflammatory mechanisms are etiologically linked to pancreatic adenocarcinoma.
人们越来越意识到,炎症在许多疾病中起着促成作用,包括胰腺癌的发生。炎症状态的特征是活性氧的产生和细胞周期的诱导,以促进组织生长和修复。肿瘤的发生、促进和扩展可能受到炎症反应中许多功能成分的影响。公认的胰腺癌危险因素包括吸烟、慢性/遗传性胰腺炎、肥胖和 2 型糖尿病。每个危险因素的共同点是,炎症状态显著驱动其病理学发展。本文将概述炎症机制如何与胰腺腺癌在病因学上相关联。