Inflammatory macrophages in pancreatic acinar cell metaplasia and initiation of pancreatic cancer
Author(s) -
GeouYarh Liou,
Peter Störz
Publication year - 2015
Publication title -
oncoscience
Language(s) - English
Resource type - Journals
ISSN - 2331-4737
DOI - 10.18632/oncoscience.151
Subject(s) - pancreatic cancer , pancreatitis , pdx1 , metaplasia , kras , pancreatic duct , acinar cell , cancer research , pancreas , pathogenesis , pathology , medicine , biology , cancer , colorectal cancer , islet , insulin
The roles of inflammatory macrophages in pancreatic tissue and the development of pancreatic cancer have not been well characterized. Recently it was shown that inflammatory macrophages, besides their function in clearing dead cells, also initiate pancreatic acinar cell metaplasia to duct-like progenitor cells. While in pancreatitis this is a reversible process, in context of an oncogenic stimulus this process is irreversible and can lead to the formation of precancerous lesions. Recent work now indicates that acquisition of an activating Kras mutation in acinar cells initiates signaling that leads to chemoattraction of M1-poliarized macrophages. This oncogene-caused chronic microinflammation can accelerate the pathogenesis of pancreatic cancers.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom