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Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer
BACKGROUND: Costimulatory signaling has been implicated as a potential regulator of antitumor immunity in various human cancers. In contrast to the negative prognostic value of aberrant B7-H1 expression by pancreatic cancer cells, the role of B7-H3 is still unknown. Therefore, we investigated the ex...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808322/ https://www.ncbi.nlm.nih.gov/pubmed/20035626 http://dx.doi.org/10.1186/1471-2407-9-463 |
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author | Loos, Martin Hedderich, Dennis M Ottenhausen, Malte Giese, Nathalia A Laschinger, Melanie Esposito, Irene Kleeff, Jörg Friess, Helmut |
author_facet | Loos, Martin Hedderich, Dennis M Ottenhausen, Malte Giese, Nathalia A Laschinger, Melanie Esposito, Irene Kleeff, Jörg Friess, Helmut |
author_sort | Loos, Martin |
collection | PubMed |
description | BACKGROUND: Costimulatory signaling has been implicated as a potential regulator of antitumor immunity in various human cancers. In contrast to the negative prognostic value of aberrant B7-H1 expression by pancreatic cancer cells, the role of B7-H3 is still unknown. Therefore, we investigated the expression pattern and clinical significance of B7-H3 expression in human pancreatic cancer. METHODS: B7-H3 expression was evaluated by immunohistochemistry in 68 patients with pancreatic cancer who underwent surgical tumor resection. Expression data was correlated with clinicopathologic features and with the number of tumor-infiltrating T cells. RESULTS: B7-H3 expression was significantly upregulated in pancreatic cancer compared to normal pancreas (p < 0.05). In 60 of 68 examined tumors B7-H3 protein was detectable in pancreatic cancer cells. Patients with high tumor B7-H3 levels had a significantly better postoperative prognosis than patients with low tumor B7-H3 levels (p = 0.0067). Furthermore, tumor B7-H3 expression significantly correlated with the number of tumor-infiltrating CD8+ T cells (p = 0.018). CONCLUSION: We demonstrate for the first time that B7-H3 is abundantly expressed in pancreatic cancer and that tumor-associated B7-H3 expression significantly correlates with prolonged postoperative survival. Our findings suggest that B7-H3 might play an important role as a potential stimulator of antitumor immune response in pancreatic cancer. |
format | Text |
id | pubmed-2808322 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28083222010-01-20 Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer Loos, Martin Hedderich, Dennis M Ottenhausen, Malte Giese, Nathalia A Laschinger, Melanie Esposito, Irene Kleeff, Jörg Friess, Helmut BMC Cancer Research Article BACKGROUND: Costimulatory signaling has been implicated as a potential regulator of antitumor immunity in various human cancers. In contrast to the negative prognostic value of aberrant B7-H1 expression by pancreatic cancer cells, the role of B7-H3 is still unknown. Therefore, we investigated the expression pattern and clinical significance of B7-H3 expression in human pancreatic cancer. METHODS: B7-H3 expression was evaluated by immunohistochemistry in 68 patients with pancreatic cancer who underwent surgical tumor resection. Expression data was correlated with clinicopathologic features and with the number of tumor-infiltrating T cells. RESULTS: B7-H3 expression was significantly upregulated in pancreatic cancer compared to normal pancreas (p < 0.05). In 60 of 68 examined tumors B7-H3 protein was detectable in pancreatic cancer cells. Patients with high tumor B7-H3 levels had a significantly better postoperative prognosis than patients with low tumor B7-H3 levels (p = 0.0067). Furthermore, tumor B7-H3 expression significantly correlated with the number of tumor-infiltrating CD8+ T cells (p = 0.018). CONCLUSION: We demonstrate for the first time that B7-H3 is abundantly expressed in pancreatic cancer and that tumor-associated B7-H3 expression significantly correlates with prolonged postoperative survival. Our findings suggest that B7-H3 might play an important role as a potential stimulator of antitumor immune response in pancreatic cancer. BioMed Central 2009-12-26 /pmc/articles/PMC2808322/ /pubmed/20035626 http://dx.doi.org/10.1186/1471-2407-9-463 Text en Copyright ©2009 Loos et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Loos, Martin Hedderich, Dennis M Ottenhausen, Malte Giese, Nathalia A Laschinger, Melanie Esposito, Irene Kleeff, Jörg Friess, Helmut Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer |
title | Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer |
title_full | Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer |
title_fullStr | Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer |
title_full_unstemmed | Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer |
title_short | Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer |
title_sort | expression of the costimulatory molecule b7-h3 is associated with prolonged survival in human pancreatic cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808322/ https://www.ncbi.nlm.nih.gov/pubmed/20035626 http://dx.doi.org/10.1186/1471-2407-9-463 |
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