| Literature DB >> 23981573 |
Andreia V Pinho1, Lorraine Chantrill2, Ilse Rooman3.
Abstract
Chronic pancreatitis predisposes to pancreatic cancer development and both diseases share a common etiology. A central role has been proposed for the digestive enzyme-secreting acinar cell that can undergo ductal metaplasia in the inflammatory environment of pancreatitis. This metaplastic change is now a recognised precursor of pancreatic cancer. Inflammatory molecules also foster tumour growth through autocrine and paracrine effects in the epithelium and the stroma. These insights have raised new opportunities such as the manipulation of inflammation as a preventive and/or therapeutic strategy for pancreatic cancer. Finally, we address the need for an in-depth study of the pancreatic acinar cells.Entities:
Keywords: Acinar to ductal metaplasia; Dedifferentiation; Inflammation; Oxidative stress; Pancreatic cancer; Pancreatitis
Mesh:
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Year: 2013 PMID: 23981573 DOI: 10.1016/j.canlet.2013.08.015
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679