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胰腺腺泡细胞化生中的炎性巨噬细胞与胰腺癌的起始

Inflammatory macrophages in pancreatic acinar cell metaplasia and initiation of pancreatic cancer.

作者信息

Liou Geou-Yarh, Storz Peter

机构信息

Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Mayo Clinic, Jacksonville, Florida, USA.

出版信息

Oncoscience. 2015 Mar 28;2(3):247-51. doi: 10.18632/oncoscience.151. eCollection 2015.

Abstract

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.

摘要

炎症性巨噬细胞在胰腺组织中的作用以及胰腺癌的发展尚未得到充分阐明。最近有研究表明,炎症性巨噬细胞除了具有清除死亡细胞的功能外,还会引发胰腺腺泡细胞向导管样祖细胞的化生。在胰腺炎中,这是一个可逆过程,但在致癌刺激的情况下,这个过程是不可逆的,可能导致癌前病变的形成。最近的研究表明,腺泡细胞中激活型Kras突变的获得会引发信号传导,导致M1极化巨噬细胞的趋化作用。这种癌基因引起的慢性微炎症会加速胰腺癌的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd86/4394130/054bf764523e/oncoscience-02-0247-g001.jpg

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