Conflict of Interest: No conflict of interest has been declared by the authors.
Dangerous liaisons: Pancreatic stellate cells and pancreatic cancer cells
Version of Record online: 9 FEB 2012
© 2012 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Special Issue: 6th International Symposium on Alcoholic Liver and Pancreatic Diseases and Cirrhosis, 20-21 October 2011, Fukuoka, Japan
Volume 27, Issue Supplement s2, pages 69–74, March 2012
How to Cite
Apte, M. V. and Wilson, J. S. (2012), Dangerous liaisons: Pancreatic stellate cells and pancreatic cancer cells. Journal of Gastroenterology and Hepatology, 27: 69–74. doi: 10.1111/j.1440-1746.2011.07000.x
- Issue online: 9 FEB 2012
- Version of Record online: 9 FEB 2012
- Accepted for publication 26 October 2011.
- pancreatic cancer;
- pancreatic stellate cells;
- tumor-stromal interactions
One of the characteristic features of the majority of pancreatic ductal adenocarcinomas is an abundant desmoplastic/stromal reaction. Until recently, this stroma had received little attention from researchers studying the pathogenesis of pancreatic cancer, with most of the research focus resting on the biology of tumor cells themselves. However, evidence is now accumulating that the stroma plays a critical role in pancreatic cancer progression. The cells responsible for producing the stromal reaction in pancreatic cancer are activated pancreatic stellate cells (PSCs, the key effector cells in pancreatic fibrogenesis). In vitro and in vivo studies have convincingly demonstrated a close bi-directional interaction between PSCs and pancreatic cancer cells, which facilitates local tumor growth as well as distant metastasis. PSCs also interact closely with endothelial cells to stimulate angiogenesis and are possibly involved in the known resistance of pancreatic cancer to chemotherapy and radiation. Most interestingly, it has recently been shown that PSCs from the primary tumor can travel to distant metastatic sites where they likely facilitate the seeding, survival, and proliferation of cancer cells. Thus, it is now recognized that the stroma is an important alternative therapeutic target in this disease and concerted pre-clinical research is underway to develop strategies to modulate/deplete the stromal reaction to inhibit cancer progression. The challenge is to translate these developments into clinically applicable treatments for patients.