G Garcea1, A R Dennison, W P Steward, D P Berry. 1. Cancer Studies and Molecular Medicine, Robert Kilpatrick Clinical Sciences Building, The Leicester Royal Infirmary, UK. gg43@le.ac.uk
Abstract
BACKGROUND: The link between inflammation and pancreatic cancer has been observed for a number of gastrointestinal neoplasms. This review examines the role of inflammation in pancreatic carcinogenesis and how it can be utilised to develop new therapies against pancreatic cancer. METHODS: A literature review of Pubmed, Medline and Web of Science databases was undertaken using the key words, pancreatic cancer, inflammation, inducible nitric oxide, interleukins, pro-inflammatory cytokines, cyclooxygenase-2, NF-kappa B, reactive oxygen species, DNA adducts, lipoxygenases, chemoprevention. RESULTS: Epidemiological evidence and molecular studies both in vitro and in vivo all support the hypothesis that inflammation plays an important in the initiation and progression of pancreatic tumours. CONCLUSION: Sustained damage caused by chronic inflammation may precede the onset of frank malignancy by a significant interval. As such, suppression of inflammatory changes and oxidative damage, may help delay or even prevent the inception of pancreatic neoplasia. Copyright 2005 S. Karger AG, Basel and IAP.
BACKGROUND: The link between inflammation and pancreatic cancer has been observed for a number of gastrointestinal neoplasms. This review examines the role of inflammation in pancreatic carcinogenesis and how it can be utilised to develop new therapies against pancreatic cancer. METHODS: A literature review of Pubmed, Medline and Web of Science databases was undertaken using the key words, pancreatic cancer, inflammation, inducible nitric oxide, interleukins, pro-inflammatory cytokines, cyclooxygenase-2, NF-kappa B, reactive oxygen species, DNA adducts, lipoxygenases, chemoprevention. RESULTS: Epidemiological evidence and molecular studies both in vitro and in vivo all support the hypothesis that inflammation plays an important in the initiation and progression of pancreatic tumours. CONCLUSION:Sustained damage caused by chronic inflammation may precede the onset of frank malignancy by a significant interval. As such, suppression of inflammatory changes and oxidative damage, may help delay or even prevent the inception of pancreatic neoplasia. Copyright 2005 S. Karger AG, Basel and IAP.
Authors: M M Gaida; F Günther; C Wagner; H Friess; N A Giese; J Schmidt; G M Hänsch; M N Wente Journal: Clin Exp Immunol Date: 2008-09-05 Impact factor: 4.330
Authors: Rachael Z Stolzenberg-Solomon; Stephanie Weinstein; Michael Pollak; Yuzhen Tao; Philip R Taylor; Jarmo Virtamo; Demetrius Albanes Journal: Am J Epidemiol Date: 2008-09-18 Impact factor: 4.897
Authors: Naotake Funamizu; Chaoxin Hu; Curtis Lacy; Aaron Schetter; Geng Zhang; Peijun He; Jochen Gaedcke; Michael B Ghadimi; Thomas Ried; Harris G Yfantis; Dong H Lee; Jeffrey Subleski; Tim Chan; Jonathan M Weiss; Timothy C Back; Katsuhiko Yanaga; Nader Hanna; H Richard Alexander; Anirban Maitra; S Perwez Hussain Journal: Int J Cancer Date: 2013-02-15 Impact factor: 7.396
Authors: Brian M Wolpin; Andrew T Chan; Patricia Hartge; Stephen J Chanock; Peter Kraft; David J Hunter; Edward L Giovannucci; Charles S Fuchs Journal: J Natl Cancer Inst Date: 2009-03-10 Impact factor: 13.506