title: Expression of cyclooxygenase-2 and vascular endothelial growth factor in pancreatic tumors.
abstract: Cyclooxygenase (COX)-2 and vascular endothelial growth factor (VEGF) have been reported to be significantly related to carcinogenesis or progression of various cancers. However, there has been no report on the relation between COX-2 and VEGF overexpression in pancreatic tumors. We investigated the overexpression of COX-2 and VEGF immunohistochemically in intraductal papillary-mucinous tumors (IPMT) and invasive ductal carcinoma (IDC) and examined the relationship with clinicopathological factors and the correlation between these immunoactivities in IPMT and IDC. In IPMT, the positive rates of COX-2 overexpression were 0% in 10 areas of hyperplasia, 54.5% of adenoma, 83.3% of intraductal areas of adenocarcinoma, and 66.7% of invasive areas of adenocarcinoma. On the contrary, 47.8% of IDC were positive for COX-2 overexpression. The positive rates of VEGF in IPMT were 10% in areas of hyperplasia, 54.5% of adenoma, 66.7% of intraductal areas of adenocarcinoma and 66.7% of invasive areas of adenocarcinoma. However, in IDC it was 47.8%. Only lymph node metastasis correlated significantly with VEGF overexpression (p=0.04), while the other factors had no significant relationships with either COX-2 or VEGF overexpression. There was a statistically significant correlation between COX-2 and VEGF overexpression in IPMT (p<0.001), in 5 patients with adenoma of which both COX-2 and VEGF were stained in almost exactly the same locations. On the contrary, COX-2 and VEGF overexpression had no statistically significant relationship in IDC. In conclusion, we demonstrate evidence of COX-2 and VEGF overexpression in human pancreatic tumors. Chemoprevention via the suppression of angiogenesis by means of COX-2 inhibitor may be more effective in IPMT than in IDC, because of the strong correlation of both factors especially in IPMT.
authors.affiliation: Department of Surgery, Tokyo Medical University, Tokyo, Japan.
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Aoki
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Nagakawa
authors.forename: Akihiko
authors.initials: A
authors.lastname: Tsuchida
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Kasuya
authors.forename: Keiichi
authors.initials: K
authors.lastname: Kitamura
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Takashi
authors.initials: T
authors.lastname: Ozawa
authors.forename: Yasuhisa
authors.initials: Y
authors.lastname: Koyanagi
authors.forename: Takao
authors.initials: T
authors.lastname: Itoi
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology / Q000473:pathology; D002288:Adenocarcinoma, Mucinous / Q000201:enzymology / Q000473:pathology; D000236:Adenoma / Q000201:enzymology / Q000473:pathology; D021441:Carcinoma, Pancreatic Ductal / Q000201:enzymology / Q000473:pathology; D051546:Cyclooxygenase 2; D016228:Endothelial Growth Factors / Q000378:metabolism*; D006801:Humans; D007124:Immunoenzyme Techniques; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D007527:Isoenzymes / Q000378:metabolism*; D008207:Lymphatic Metastasis; D008222:Lymphokines / Q000378:metabolism*; D008565:Membrane Proteins; D009361:Neoplasm Invasiveness; D010190:Pancreatic Neoplasms / Q000201:enzymology* / Q000473:pathology; D018300:Papilloma, Intraductal / Q000201:enzymology / Q000473:pathology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D007527:Isoenzymes; D008222:Lymphokines; D008565:Membrane Proteins; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases