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Pancreatic Cancer: The Role of Pancreatic Stellate Cells in Tumor Progression.

Dunér, Siri; Lopatko Lindman, Jacob; Ansari, Daniel LU ; Gundewar, Chinmay LU and Andersson, Roland LU (2010) In Pancreatology 10(6). p.673-681
Abstract
Pancreatic ductal adenocarcinoma is an aggressive and highly lethal disease frequently characterized by a dense stromal or desmoplastic response. Accumulating evidence exists that tumor desmoplasia plays a central role in disease progression and that e.g. activated pancreatic stellate cells (PSCs) are responsible for the excess matrix production. The mechanisms underlying the tumor versus stroma interplay are complex. Pancreatic cancer cells release mitogenic and fibrogenic stimulants, such as transforming growth factor β(1), platelet-derived growth factor (PDGF), sonic hedgehog, galectin 3, endothelin 1 and serine protease inhibitor nexin 2, all of which may promote the activated PSC phenotype. Stellate cells in turn secrete various... (More)
Pancreatic ductal adenocarcinoma is an aggressive and highly lethal disease frequently characterized by a dense stromal or desmoplastic response. Accumulating evidence exists that tumor desmoplasia plays a central role in disease progression and that e.g. activated pancreatic stellate cells (PSCs) are responsible for the excess matrix production. The mechanisms underlying the tumor versus stroma interplay are complex. Pancreatic cancer cells release mitogenic and fibrogenic stimulants, such as transforming growth factor β(1), platelet-derived growth factor (PDGF), sonic hedgehog, galectin 3, endothelin 1 and serine protease inhibitor nexin 2, all of which may promote the activated PSC phenotype. Stellate cells in turn secrete various factors, including PDGF, stromal-derived factor 1, epidermal growth factor, insulin-like growth factor 1, fibroblast growth factor, secreted protein acidic and rich in cysteine, matrix metalloproteinases, small leucine-rich proteoglycans, periostin and collagen type I that mediate effects on tumor growth, invasion, metastasis and resistance to chemotherapy. This review intends to shed light on the mechanisms by which PSCs in the stroma influence pancreatic cancer development. The increased understanding of this interaction will be of potential value in designing new modalities of targeted therapy. and IAP. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pancreatology
volume
10
issue
6
pages
673 - 681
publisher
Karger
external identifiers
  • wos:000295592200005
  • pmid:21242706
  • scopus:78651385353
ISSN
1424-3903
DOI
10.1159/000320711
language
English
LU publication?
yes
id
08341adf-f73b-4ba9-a06e-2bf83b1ef4ca (old id 1777384)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21242706?dopt=Abstract
date added to LUP
2011-02-01 14:28:39
date last changed
2018-06-10 04:47:26
@article{08341adf-f73b-4ba9-a06e-2bf83b1ef4ca,
  abstract     = {Pancreatic ductal adenocarcinoma is an aggressive and highly lethal disease frequently characterized by a dense stromal or desmoplastic response. Accumulating evidence exists that tumor desmoplasia plays a central role in disease progression and that e.g. activated pancreatic stellate cells (PSCs) are responsible for the excess matrix production. The mechanisms underlying the tumor versus stroma interplay are complex. Pancreatic cancer cells release mitogenic and fibrogenic stimulants, such as transforming growth factor β(1), platelet-derived growth factor (PDGF), sonic hedgehog, galectin 3, endothelin 1 and serine protease inhibitor nexin 2, all of which may promote the activated PSC phenotype. Stellate cells in turn secrete various factors, including PDGF, stromal-derived factor 1, epidermal growth factor, insulin-like growth factor 1, fibroblast growth factor, secreted protein acidic and rich in cysteine, matrix metalloproteinases, small leucine-rich proteoglycans, periostin and collagen type I that mediate effects on tumor growth, invasion, metastasis and resistance to chemotherapy. This review intends to shed light on the mechanisms by which PSCs in the stroma influence pancreatic cancer development. The increased understanding of this interaction will be of potential value in designing new modalities of targeted therapy. and IAP.},
  author       = {Dunér, Siri and Lopatko Lindman, Jacob and Ansari, Daniel and Gundewar, Chinmay and Andersson, Roland},
  issn         = {1424-3903},
  language     = {eng},
  number       = {6},
  pages        = {673--681},
  publisher    = {Karger},
  series       = {Pancreatology},
  title        = {Pancreatic Cancer: The Role of Pancreatic Stellate Cells in Tumor Progression.},
  url          = {http://dx.doi.org/10.1159/000320711},
  volume       = {10},
  year         = {2010},
}