Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1016/j.canlet.2013.09.039

Type

Journal article

Journal

Cancer Lett

Publication Date

28/02/2014

Volume

343

Pages

147 - 155

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, Antineoplastic Agents, Cell Compartmentation, Drug Delivery Systems, Humans, Pancreatic Neoplasms, Stromal Cells, Tumor Microenvironment