Pancreatic ductal adenocarcinoma (PDAC) is characterised by an abundant stromal response also known as a desmoplastic reaction. Pancreatic Stellate Cells have been identified as playing a key role in pancreatic cancer desmoplasia. There is accumulating evidence that the stroma contributes to tumour progression and to the low therapeutic response of PDAC patients. In this review we described the main actors of the desmoplastic reaction within PDAC and novel therapeutic approaches that are being tested to block the detrimental function of the stroma.
Keywords: COX-2; CTLs; Cytotoxic T Lymphocytes; DCs; ECM; EGF; FAK; FAP-α; FGF; HSCs; IGF-1; Insulin Growth Factor-1; MDSCs; MMP; PCCs; PDAC; PDGF; PSCs; Pancreatic Stellate Cells; Pancreatic cancer; SERBIPINE2; SHH; SPARC; Stroma; TAMs; TGF-β; TIMP; Tregs; Tumour microenvironment; VEGF; cyclooxygenase-2; dendritic cells; epidermal growth factor; extracellular matrix; fibroblast activation protein-α; fibroblast growth factor; focal adhesion kinase; hepatic stellate cell; matrix metalloproteinases; myeloid-derived suppressor cells; pancreatic cancer cells; pancreatic ductal adenocarcinoma; platelet-derived growth factor; regulatory T cells (Tregs); secreted protein acidic and rich in cysteine; serine protease inhibitor nexin 2; sonic hedgehog; tPA; tissue inhibitors of metalloproteinases; tissue plasminogen activator; transforming growth factor-β; tumour associated macrophages; uPA; urokinase-type plasminogen activator; vascular endothelial growth factor; α-SMA; α-smooth muscle actin.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.