Cyclooxygenase-2 Expression in Hamster and Human Pancreatic Neoplasia
dc.contributor.author | Crowell, Pamela L. | |
dc.contributor.author | Schmidt, C. Max | |
dc.contributor.author | Yip-Schneider, Michele T. | |
dc.contributor.author | Savage, Jesse J. | |
dc.contributor.author | Hertzler II, Dean A. | |
dc.contributor.author | Cummings, William O. | |
dc.contributor.department | Biochemistry and Molecular Biology, School of Medicine | en_US |
dc.date.accessioned | 2021-02-04T15:39:24Z | |
dc.date.available | 2021-02-04T15:39:24Z | |
dc.date.issued | 2006-06 | |
dc.description.abstract | Cyclooxygenase-2 (COX-2) has been implicated in the development of gastrointestinal malignancies. The aim of the present study was to determine COX-2 expression/activity throughout stages of experimental and human pancreatic neoplasia. COX-2 immunohistochemistry was performed in pancreata of hamsters subjected to the carcinogen N-nitrosobis-(2-oxopropyl)amine (BOP) and in human pancreatic tumors. COX-2 activity was determined by prostaglandin E2 assay in tumor versus matched normal pancreatic tissues. The activity of the COX inhibitor sulindac was tested in the PC-1 hamster pancreatic cancer model. COX-2 expression was elevated in all pancreatic intraepithelial neoplasias (PanINs) and adenocarcinomas. In BOP-treated hamsters, there were significant progressive elevations in COX-2 expression throughout pancreatic tumorigenesis. In human samples, peak COX-2 expression occurred in PanIN2 lesions and remained moderately elevated in PanIN3 and adenocarcinoma tissues. COX-2 activity was significantly elevated in hamster and human pancreatic cancers compared to pair-matched normal pancreas. Furthermore, hamster pancreatic tumor engraftment/formation in the PC-1 hamster pancreatic cancer model was reduced 4.9-fold by oral administration of sulindac. Increased COX-2 expression is an early event in pancreatic carcinogeneses. The BOP-induced hamster carcinogenesis model is a representative model used to study the role of COX-2 in well-differentiated pancreatic tumorigenesis. COX inhibitors may have a role in preventing tumor engraftment/formation. | en_US |
dc.eprint.version | Final published version | en_US |
dc.identifier.citation | Crowell, P. L., Schmidt, C. M., Yip-Schneider, M. T., Savage, J. J., Hertzler II, D. A., & Cummings, W. O. (2006). Cyclooxygenase-2 expression in hamster and human pancreatic neoplasia. Neoplasia, 8(6), 437-445. | en_US |
dc.identifier.uri | https://hdl.handle.net/1805/25145 | |
dc.language.iso | en_US | en_US |
dc.publisher | Elsevier | en_US |
dc.relation.isversionof | 10.1593/neo.04700 | en_US |
dc.relation.journal | Neoplasia | en_US |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 International | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.source | Publisher | en_US |
dc.subject | Pancreatic neoplasms | en_US |
dc.subject | PanIN | en_US |
dc.subject | COX-2 | en_US |
dc.subject | chemical carcinogenesis | en_US |
dc.title | Cyclooxygenase-2 Expression in Hamster and Human Pancreatic Neoplasia | en_US |
dc.type | Article | en_US |
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