scholarly journals Inhibition of group 1 p21-activated kinases suppresses pancreatic stellate cell activation and increases survival of mice with pancreatic cancer

2017 ◽  
Vol 140 (9) ◽  
pp. 2101-2111 ◽  
Author(s):  
Dannel Yeo ◽  
Phoebe Phillips ◽  
Graham S. Baldwin ◽  
Hong He ◽  
Mehrdad Nikfarjam
Keyword(s):  
Pancreatic Cancer ◽  
Cell Activation ◽  
Stellate Cell ◽  
Pancreatic Stellate Cell ◽  
Group 1

scholarly journals Efficient Targeted Therapy for Pancreatic Cancer Using Nanosystem and Focusing on the Suppression of Pancreatic Stellate Cell Activation

HPB ◽  
2021 ◽  
Vol 23 ◽  
pp. S54
Author(s):  
S. Matsumoto ◽  
K. Nakata ◽  
N. Ikenaga ◽  
S. Date ◽  
W. Guan ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Targeted Therapy ◽  
Cell Activation ◽  
Stellate Cell ◽  
Pancreatic Stellate Cell

Fibrogenesis in the Pancreas after Acinar Cell Injury

2005 ◽  
Vol 94 (2) ◽  
pp. 108-111 ◽  
Author(s):  
M. Patel ◽  
D. R. Fine
Keyword(s):  
Pancreatic Cancer ◽  
Chronic Pancreatitis ◽  
Cell Activation ◽  
Cell Injury ◽  
Stellate Cell ◽  
Acinar Cells ◽  
Signalling Pathways ◽  
Phenotypic Change ◽  
Current Interest ◽  
Pancreatic Stellate Cell

Fibrosis within the pancreas is a key feature of chronic pancreatitis and pancreatic cancer. It has now been well demonstrated that following injury to acinar cells, pancreatic stellate cell activation, migration and proliferation is the key mediator of this process. Many cytokines and growth factors have been studied, particularly TGF-β, which appears to be the major stimulus to fibrinogenesis. There is current interest in the mechanisms of phenotypic change between the active and quiescent forms, apoptosis and the signalling pathways that may be involved. The pancreatic stellate cell is likely to play an important role in maintaining the normal extracellular matrix; we speculate that the dysregulation of this process is an important factor in chronic pancreatitis.

S1820 Heat Shock Proteins Are Induced During Pancreatic Stellate Cell Activation in Pancreatic Cancer

2009 ◽  
Vol 136 (5) ◽  
pp. A-277
Author(s):  
Phoebe Phillips ◽  
Lu Yang ◽  
Alain Vonlaufen ◽  
Zhihong Xu ◽  
Andrew V. Biankin ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Cell Activation ◽  
Stellate Cell ◽  
Pancreatic Stellate Cell ◽  
Shock Proteins

AB011. S011. Mesenchymal pancreatic cancer cells inhibit pancreatic stellate cell activation

2018 ◽  
Vol 1 (1) ◽  
pp. AB011-AB011
Author(s):  
Madelaine van Mackelenbergh ◽  
Anne Steins, J. W. Wilmink ◽  
Hanneke W. van Laarhoven ◽  
Maarten F. Bijlsma
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Cell Activation ◽  
Stellate Cell ◽  
Pancreatic Stellate Cell ◽  
Pancreatic Cancer Cells

1133 PANCREATIC STELLATE CELL AND CANCER CELL DERIVED EXOSOMES IMPAIR BETA CELL FUNCTION: IMPLICATIONS FOR PANCREATIC CANCER RELATED DIABETES.

2020 ◽  
Vol 158 (6) ◽  
pp. S-221
Author(s):  
Chamini Perera ◽  
Zhihong Xu ◽  
Alpha Raj Mekapogu ◽  
S.M. Zahid Hosen ◽  
Srinivasa Pothula ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Beta Cell ◽  
Cancer Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Stellate Cell ◽  
Pancreatic Stellate Cell

scholarly journals HGF/c-Met Inhibition as Adjuvant Therapy Improves Outcomes in an Orthotopic Mouse Model of Pancreatic Cancer

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2763
Author(s):  
Tony C. Y. Pang ◽  
Zhihong Xu ◽  
Alpha Raj Mekapogu ◽  
Srinivasa Pothula ◽  
Therese Becker ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Primary Tumour ◽  
Human Pancreatic Cancer ◽  
Pancreatic Stellate Cell ◽  
Orthotopic Mouse Model ◽  
Pancreatic Cancer Cells ◽  
Angiogenic Effect

Background: Inhibition of hepatocyte growth factor (HGF)/c-MET pathway, a major mediator of pancreatic stellate cell (PSC)−PC cell interactions, retards local and distant cancer progression. This study examines the use of this treatment in preventing PC progression after resection. We further investigate the postulated existence of circulating PSCs (cPSCs) as a mediator of metastatic PC. Methods: Two orthotopic PC mouse models, produced by implantation of a mixture of luciferase-tagged human pancreatic cancer cells (AsPC-1), and human PSCs were used. Model 1 mice underwent distal pancreatectomy 3-weeks post-implantation (n = 62). One-week post-resection, mice were randomised to four treatments of 8 weeks: (i) IgG, (ii) gemcitabine (G), (iii) HGF/c-MET inhibition (HiCi) and (iv) HiCi + G. Tumour burden was assessed longitudinally by bioluminescence. Circulating tumour cells and cPSCs were enriched by filtration. Tumours of Model 2 mice progressed for 8 weeks prior to the collection of primary tumour, metastases and blood for single-cell RNA-sequencing (scRNA-seq). Results: HiCi treatments: (1) reduced both the risk and rate of disease progression after resection; (2) demonstrated an anti-angiogenic effect on immunohistochemistry; (3) reduced cPSC counts. cPSCs were identified using immunocytochemistry (α-smooth muscle actin+, pan-cytokeratin−, CD45−), and by specific PSC markers. scRNA-seq confirmed the existence of cPSCs and identified potential genes associated with development into cPSCs. Conclusions: This study is the first to demonstrate the efficacy of adjuvant HGF/c-Met inhibition for PC and provides the first confirmation of the existence of circulating PSCs.

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