Abstract
Our understanding of pancreatic ductal adenocarcinoma (PDAC) is shifting away from a disease of malignant ductal cells-only, toward a complex system where tumor evolution is a result of interaction of cancer cells with their microenvironment. This change has led to intensification of research focusing on the fibrotic stroma of PDAC. Pancreatic stellate cells (PSCs) are the main fibroblastic cells of the pancreas which are responsible for producing the desmoplasia in chronic pancreatitis (CP) and PDAC. Clinically, the effect of desmoplasia is two-sided; on the negative side it is a hurdle in the diagnosis of PDAC because the fibrosis in cancer resembles that of CP. It is also believed that PSCs and pancreatic fibrosis are partially responsible for the therapy resistance in pancreatic cancer. On the positive side, a fibrotic pancreas is safer to operate on compared to a fatty and soft pancreas which is prone for postoperative pancreatic fistula. In this review the impact of pancreatic fibrosis on diagnosis of pancreatic cancer and surgical decisions are discussed from a clinical point of view.
Highlights
Pancreatic fibrosis is found both in chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC)
The effect of desmoplasia is two-sided; on the negative side it is a hurdle in the diagnosis of PDAC because the fibrosis in cancer resembles that of CP
We have previously shown that Pancreatic stellate cells (PSCs) are activated in vitro after radiotherapy and resected tissues of patients after radiotherapy contain acellular areas of fibrosis (Erkan et al, 2007a)
Summary
Pancreatic fibrosis (desmoplasia) is found both in chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC). PERIACINAR FIBROSIS AND CHRONIC PANCREATITIS LIKE CHANGES AROUND THE TUMOR Quiescent PSC belong to the stellate cell system consisting of retinoid-storing cells in various organs (Erkan et al, 2012a) In the pancreas, they are located in the periacinar spaces in close proximity to the basal aspect of acinar cells, capillaries, and terminal nerve fibers (Samkharadze et al, 2011; Apte and Wilson, 2012). Judging by early activation markers like periostin, one can observe in pancreatic diseases that the initial activation of quiescent PSC and extracellular matrix (ECM) deposition takes place in the periacinar spaces (Erkan et al, 2009, 2012c) This type of CP-like changes surround the tumor like an umbra and infiltrate the normal parenchyma (Figures 1C,D). It is likely that deposition of ECM around the capillaries and nerve endings www.frontiersin.org
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