TY  - JOUR
  - Bennett, M. W.,O'Connell, J.,O'Sullivan, G. C.,Roche, D.,Brady, C.,Kelly, J.,Collins, J. K.,Shanahan, F.
  - 1999
  - February
  - Gut
  - Expression of Fas ligand by human gastric adenocarcinomas: a potential mechanism of immune escape in stomach cancer
  - Validated
  - ()
  - 44
  - 2
  - 156
  - 162
  - Background-Despite being immunogenic, gastric cancers overcome antitumour immune responses by mechanisms that have yet to be fully elucidated. Fas ligand (FasL) is a molecule that induces Fas receptor mediated apoptosis of activated immunocytes, thereby mediating normal immune downregulatory roles including immune response termination, tolerance acquisition, and immune privilege. Colon cancer cell lines have previously been shown to express Fast and kill lymphoid cells by Fas mediated apoptosis in vitro. Many diverse tumours have since been found to express Fast suggesting that a "Fas counterattack" against antitumour immune effector cells may contribute to tumour immune escape. Aim-To ascertain if human gastric tumours express Fast in vivo, as a potential mediator of immune escape in stomach cancer. Specimens-Thirty paraffin wax embedded human gastric adenocarcinomas. Methods-FasL protein was detected in gastric tumours using immunohistochemistry; Fast mRNA was detected in the tumours using in situ hybridisation. Cell death was detected in situ in tumour infiltrating lymphocytes using terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Results-Prevalent expression of Fast was detected in all 30 resected gastric adenocarcinomas examined. In the tumours, Fast protein and mRNA were co-localised to neoplastic gastric epithelial cells, confirming expression by the tumour cells. Fast expression was independent of tumour stage, suggesting that it may be expressed throughout gastric cancer progression. TUNEL staining disclosed a high level of cell death among lymphocytes infiltrating Fast positive areas of tumour. Conclusions-Human gastric adenocarcinomas express the immune downregulatory molecule, Fast. The results suggest that Fast is a prevalent mediator of immune privilege in stomach cancer.Background-Despite being immunogenic, gastric cancers overcome antitumour immune responses by mechanisms that have yet to be fully elucidated. Fas ligand (FasL) is a molecule that induces Fas receptor mediated apoptosis of activated immunocytes, thereby mediating normal immune downregulatory roles including immune response termination, tolerance acquisition, and immune privilege. Colon cancer cell lines have previously been shown to express Fast and kill lymphoid cells by Fas mediated apoptosis in vitro. Many diverse tumours have since been found to express Fast suggesting that a "Fas counterattack" against antitumour immune effector cells may contribute to tumour immune escape. Aim-To ascertain if human gastric tumours express Fast in vivo, as a potential mediator of immune escape in stomach cancer. Specimens-Thirty paraffin wax embedded human gastric adenocarcinomas. Methods-FasL protein was detected in gastric tumours using immunohistochemistry; Fast mRNA was detected in the tumours using in situ hybridisation. Cell death was detected in situ in tumour infiltrating lymphocytes using terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Results-Prevalent expression of Fast was detected in all 30 resected gastric adenocarcinomas examined. In the tumours, Fast protein and mRNA were co-localised to neoplastic gastric epithelial cells, confirming expression by the tumour cells. Fast expression was independent of tumour stage, suggesting that it may be expressed throughout gastric cancer progression. TUNEL staining disclosed a high level of cell death among lymphocytes infiltrating Fast positive areas of tumour. Conclusions-Human gastric adenocarcinomas express the immune downregulatory molecule, Fast. The results suggest that Fast is a prevalent mediator of immune privilege in stomach cancer.
  - 0017-57490017-5749
  - ://WOS:000078181200008://WOS:000078181200008
DA  - 1999/02
ER  - 

@article{V235379806,
   = {Bennett,  M. W. and O'Connell,  J. and O'Sullivan,  G. C. and Roche,  D. and Brady,  C. and Kelly,  J. and Collins,  J. K. and Shanahan,  F. },
   = {1999},
   = {February},
   = {Gut},
   = {Expression of Fas ligand by human gastric adenocarcinomas: a potential mechanism of immune escape in stomach cancer},
   = {Validated},
   = {()},
   = {44},
   = {2},
  pages = {156--162},
   = {{Background-Despite being immunogenic, gastric cancers overcome antitumour immune responses by mechanisms that have yet to be fully elucidated. Fas ligand (FasL) is a molecule that induces Fas receptor mediated apoptosis of activated immunocytes, thereby mediating normal immune downregulatory roles including immune response termination, tolerance acquisition, and immune privilege. Colon cancer cell lines have previously been shown to express Fast and kill lymphoid cells by Fas mediated apoptosis in vitro. Many diverse tumours have since been found to express Fast suggesting that a "Fas counterattack" against antitumour immune effector cells may contribute to tumour immune escape. Aim-To ascertain if human gastric tumours express Fast in vivo, as a potential mediator of immune escape in stomach cancer. Specimens-Thirty paraffin wax embedded human gastric adenocarcinomas. Methods-FasL protein was detected in gastric tumours using immunohistochemistry; Fast mRNA was detected in the tumours using in situ hybridisation. Cell death was detected in situ in tumour infiltrating lymphocytes using terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Results-Prevalent expression of Fast was detected in all 30 resected gastric adenocarcinomas examined. In the tumours, Fast protein and mRNA were co-localised to neoplastic gastric epithelial cells, confirming expression by the tumour cells. Fast expression was independent of tumour stage, suggesting that it may be expressed throughout gastric cancer progression. TUNEL staining disclosed a high level of cell death among lymphocytes infiltrating Fast positive areas of tumour. Conclusions-Human gastric adenocarcinomas express the immune downregulatory molecule, Fast. The results suggest that Fast is a prevalent mediator of immune privilege in stomach cancer.Background-Despite being immunogenic, gastric cancers overcome antitumour immune responses by mechanisms that have yet to be fully elucidated. Fas ligand (FasL) is a molecule that induces Fas receptor mediated apoptosis of activated immunocytes, thereby mediating normal immune downregulatory roles including immune response termination, tolerance acquisition, and immune privilege. Colon cancer cell lines have previously been shown to express Fast and kill lymphoid cells by Fas mediated apoptosis in vitro. Many diverse tumours have since been found to express Fast suggesting that a "Fas counterattack" against antitumour immune effector cells may contribute to tumour immune escape. Aim-To ascertain if human gastric tumours express Fast in vivo, as a potential mediator of immune escape in stomach cancer. Specimens-Thirty paraffin wax embedded human gastric adenocarcinomas. Methods-FasL protein was detected in gastric tumours using immunohistochemistry; Fast mRNA was detected in the tumours using in situ hybridisation. Cell death was detected in situ in tumour infiltrating lymphocytes using terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL). Results-Prevalent expression of Fast was detected in all 30 resected gastric adenocarcinomas examined. In the tumours, Fast protein and mRNA were co-localised to neoplastic gastric epithelial cells, confirming expression by the tumour cells. Fast expression was independent of tumour stage, suggesting that it may be expressed throughout gastric cancer progression. TUNEL staining disclosed a high level of cell death among lymphocytes infiltrating Fast positive areas of tumour. Conclusions-Human gastric adenocarcinomas express the immune downregulatory molecule, Fast. The results suggest that Fast is a prevalent mediator of immune privilege in stomach cancer.}},
  issn = {0017-57490017-5749},
   = {://WOS:000078181200008://WOS:000078181200008},
  source = {IRIS}
}