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- Document type:
- Journal Article; Article
- Author(s):
- Loos, M; Hedderich, DM; Ottenhausen, M; Giese, NA; Laschinger, M; Esposito, I; Kleeff, J; Friess, H
- Title:
- Expression of the costimulatory molecule B7-H3 is associated with prolonged survival in human pancreatic cancer.
- Abstract:
- 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.
- Journal title abbreviation:
- BMC Cancer
- Year:
- 2009
- Journal volume:
- 9
- Pages contribution:
- 463
- Language:
- eng
- Fulltext / DOI:
- doi:10.1186/1471-2407-9-463
- Pubmed ID:
- http://view.ncbi.nlm.nih.gov/pubmed/20035626
- TUM Institution:
- Chirurgische Klinik und Poliklinik; Institut für Allgemeine Pathologie und Pathologische Anatomie
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