Expression of the Novel Costimulatory Molecule B7-H5 in Pancreatic Cancer

• Published in: Annals of surgical oncology 2015-12, Vol.22 (Suppl 3), p.1574-1579
• Main Authors: Byers, Joshua T., Paniccia, Alessandro, Kaplan, Jeffrey, Koenig, Michelle, Kahn, Nate, Wilson, Lora, Chen, Lieping, Schulick, Richard D., Edil, Barish H., Zhu, Yuwen
• Format: Article
• Language: English
• Subjects: Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Biomarkers, Tumor - metabolism; Carcinoma, Pancreatic Ductal - metabolism; Carcinoma, Pancreatic Ductal - pathology; Flow Cytometry; Gene Expression Regulation, Neoplastic; Humans; Immunoenzyme Techniques; Immunoglobulins - metabolism; Medicine; Medicine & Public Health; Neoplasm Staging; Oncology; Pancreas - metabolism; Pancreas - pathology; Pancreatic cancer; Pancreatic Neoplasms - metabolism; Pancreatic Neoplasms - pathology; Prognosis; Surgery; Surgical Oncology; Translational Research and Biomarkers; Tumor Cells, Cultured
• ISSN: 1068-9265; 1534-4681
• DOI: 10.1245/s10434-014-4293-2

Background This study investigated how the B7-H5 protein, a new member of the B7 family, is expressed in normal human pancreas tissues and examined its expression changes in pancreatic cancer. Methods In this analysis, B7-H5 expression was examined by immunohistochemical staining of frozen specimens from patients undergoing pancreatic resection. Results Membranous B7-H5 protein was expressed on normal ductal epithelium within the pancreas. Other cell types from the normal pancreas, such as acinar cells and islet cells, did not express B7-H5. In adenocarcinoma, B7-H5 staining was decreased or absent. Interestingly, B7-H5 expression in intraductal papillary mucinous neoplasms varied with grade. No B7-H5 expression was found with other cancer types such as neuroendocrine tumors, but normal ducts adjacent to tumors were highly positive. Conclusions The findings showed that B7-H5 expression was restricted to ductal cells in the normal pancreas and the expression was downregulated in pancreatic adenocarcinomas. In addition, the findings showed that B7-H5 expression changes within different stages of dysplasia. The study suggests that loss of the B7-H5 signal may contribute to immune evasion of pancreatic adenocarcinoma. However future studies are needed.