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Pancreatic Neoplasms: HELP
Articles by Alain Vonlaufen
Based on 3 articles published since 2008
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Between 2008 and 2019, Alain Vonlaufen wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Pancreatic stellate cells and pancreatic cancer cells: an unholy alliance. 2008

Vonlaufen, Alain / Phillips, Phoebe A / Xu, Zhihong / Goldstein, David / Pirola, Romano C / Wilson, Jeremy S / Apte, Minoti V. ·Pancreatic Research Group, South Western Sydney Clinical School and School of Medical Sciences/Pathology, The University of New South Wales and Sydney, Sydney, NSW, Australia. ·Cancer Res · Pubmed #18829522.

ABSTRACT: Pancreatic cancer--a tumor displaying a particularly abundant stromal reaction--is notorious for its poor prognosis. Recent studies, via newly developed orthotopic models, provide compelling evidence of an important role for pancreatic stellate cells (PSC) in pancreatic cancer progression. Characterization of the mechanisms mediating PSC-cancer interactions will lead to the development of much needed alternative therapeutic approaches to improve disease outcome.

2 Article Role of pancreatic stellate cells in pancreatic cancer metastasis. 2010

Xu, Zhihong / Vonlaufen, Alain / Phillips, Phoebe A / Fiala-Beer, Eva / Zhang, Xuguo / Yang, Lu / Biankin, Andrew V / Goldstein, David / Pirola, Romano C / Wilson, Jeremy S / Apte, Minoti V. ·Pancreatic Research Group, South Western Sydney Clinical School, School of Medical Sciences, Faculty of Medicine, Room 505, Level 5, Wallace Wurth Building, The University of New South Wales, Sydney, NSW 2052, Australia. ·Am J Pathol · Pubmed #20934972.

ABSTRACT: Pancreatic stellate cells (PSCs) produce the stromal reaction in pancreatic cancer (PC), and their interaction with cancer cells facilitates cancer progression. This study investigated the role of human PSCs (hPSCs) in the metastatic process and tumor angiogenesis using both in vivo (orthotopic model) and in vitro (cultured PSC and PC cells) approaches. A sex mismatch study (injection of male hPSCs plus female PC cells into the pancreas of female mice) was conducted to determine whether hPSCs accompany cancer cells to metastatic sites. Metastatic nodules were examined by fluorescent in situ hybridization for the presence of the Y chromosome. Angiogenesis was assessed by i) immunostaining tumors for CD31, an endothelial cell marker; and ii) quantifying human microvascular endothelial cell (HMEC-1) tube formation in vitro on exposure to conditioned media from hPSCs. Transendothelial migration was assessed in vitro by examining the movement of fluorescently labeled hPSCs through an endothelial cell monolayer. Human PSCs i) were found in multiple metastatic sites in each mouse injected with male hPSCs plus female PC cells; ii) increased CD31 expression in primary tumors from mice injected with MiaPaCa-2 and hPSCs and stimulated tube formation by HMEC-1 in vitro; and iii) exhibited transendothelial migration that was stimulated by cancer cells. Human PSCs accompany cancer cells to metastatic sites, stimulate angiogenesis, and are able to intravasate/extravasate to and from blood vessels.

3 Article Pancreatic stellate cells: partners in crime with pancreatic cancer cells. 2008

Vonlaufen, Alain / Joshi, Swapna / Qu, Changfa / Phillips, Phoebe A / Xu, Zhihong / Parker, Nicole R / Toi, Cheryl S / Pirola, Romano C / Wilson, Jeremy S / Goldstein, David / Apte, Minoti V. ·Pancreatic Research Group, South Western Sydney Clinical School, The University of New South Wales, Sydney, New South Wales 2052, Australia. ·Cancer Res · Pubmed #18381413.

ABSTRACT: Pancreatic stellate cells (PSC) produce the stromal reaction in pancreatic cancer, but their role in cancer progression is not fully elucidated. We examined the influence of PSCs on pancreatic cancer growth using (a) an orthotopic model of pancreatic cancer and (b) cultured human PSCs (hPSC) and human pancreatic cancer cell lines MiaPaCa-2 and Panc-1. Athymic mice received an intrapancreatic injection of saline, hPSCs, MiaPaCa-2 cells, or hPSCs + MiaPaCa-2. After 7 weeks, tumor size, metastases, and tumor histology were assessed. In vitro studies assessed the effect of cancer cell secretions on PSC migration and the effect of hPSC secretions on cancer cell proliferation, apoptosis, and migration. Possible mediators of the effects of hPSC secretions on cancer cell proliferation were examined using neutralizing antibodies. Compared with mice receiving MiaPaCa-2 cells alone, mice injected with hPSCs + MiaPaCa-2 exhibited (a) increased tumor size and regional and distant metastasis, (b) fibrotic bands (desmoplasia) containing activated PSCs within tumors, and (c) increased tumor cell numbers. In vitro studies showed that, in the presence of pancreatic cancer cells, PSC migration was significantly increased. Furthermore, hPSC secretions induced the proliferation and migration, but inhibited the apoptosis, of MiaPaCa-2 and Panc-1 cells. The proliferative effect of hPSC secretions on pancreatic cancer cells was inhibited in the presence of neutralizing antibody to platelet-derived growth factor. Our studies indicate a significant interaction between pancreatic cancer cells and stromal cells (PSCs) and imply that pancreatic cancer cells recruit stromal cells to establish an environment that promotes cancer progression.