Abstract
Pancreatic cancer is a complex, aggressive, and heterogeneous malignancy driven by the multifaceted interactions within the tumor microenvironment. While it is known that the tumor microenvironment accommodates many cell types, each playing a key role in tumorigenesis, the major source of these stromal cells is not well-understood. This review examines the contribution of bone marrow-derived cells (BMDC) to pancreatic carcinogenesis, with respect to their role in constituting the tumor microenvironment. In particular, their role in supporting fibrosis, immunosuppression, and neovascularization will be discussed.
Highlights
It is long known that adult stem cells have remarkable flexibility in their differentiation repertoires
In chronic pancreatitis, Bone marrow derived cells (BMDC) contribute significantly to the activated pancreatic stellate cell (PSC) population, with evidence suggesting that this process occurs as an early event in pancreatic carcinogenesis (Scarlett et al, 2011). Those associated with pancreatic cancer express genes characteristic of peritumoral stellate cells as compared to those not associated with malignancy, providing further evidence that BMDC play an important role in supporting pancreatic carcinogenesis, the mechanisms of which remain to be elucidated
The importance of an additional immunosuppressive cell type within the stroma was further defined through a recent study by Kraman et al (2010), who demonstrated that a sub-population of stromal cells that express fibroblast activation protein (FAP) suppress the immune response and that abrogation of Fibroblast activating protein (FAP) expression arrests the growth of pancreatic tumors, potentially by removing their inhibitory effect on the host’s immune response. (Kraman et al, 2010; Schreiber and Rowley, 2010)
Summary
It is long known that adult stem cells have remarkable flexibility in their differentiation repertoires. These data suggest that while BMDC do not contribute directly to pancreatic epithelial tumorigenesis, they play a significant and supportive role in promoting carcinogenesis via interactions within the tumor microenvironment.
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