Expression of inducible nitric oxide synthase and cyclooxygenase-2 in pancreatic adenocarcinoma: correlation with microvessel density

Cyclooxygenases (COX) are key enzymes for conversion of arachidonic acid to prostaglandins. Nitric oxide synthase (NOS) is the enzyme responsible for formation of nitric oxide. Both have constitutive and inducible isoforms. The inducible isoforms (iNOS and COX-2) are of great interest as regulators...

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Published in:World journal of gastroenterology : WJG 2004-07, Vol.10 (13), p.1918-1922
Main Authors: Kasper, Hans-U, Wolf, Hella, Drebber, Uta, Wolf, Helmut-K, Kern, Michael-A
Format: Article
Language:English
Subjects:
Adenocarcinoma - blood supply
Adenocarcinoma - metabolism
Adenocarcinoma - pathology
Aged
Aged, 80 and over
Basic Research
Cyclooxygenase 2
Female
Humans
Immunohistochemistry
Isoenzymes - metabolism
Male
Membrane Proteins
Microcirculation
Middle Aged
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Pancreas - blood supply
Pancreas - enzymology
Pancreas - pathology
Pancreatic Neoplasms - blood supply
Pancreatic Neoplasms - metabolism
Pancreatic Neoplasms - pathology
Prostaglandin-Endoperoxide Synthases - metabolism
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Summary:Cyclooxygenases (COX) are key enzymes for conversion of arachidonic acid to prostaglandins. Nitric oxide synthase (NOS) is the enzyme responsible for formation of nitric oxide. Both have constitutive and inducible isoforms. The inducible isoforms (iNOS and COX-2) are of great interest as regulators of tumor angiogenesis, tumorigenesis and inflammatory processes. This study was to clarify their role in pancreatic adenocarcinomas. We investigated the immunohistochemical iNOS and COX-2 expression in 40 pancreatic ductal adenocarcinomas of different grade and stage. The results were compared with microvessel density and clinicopathological data. Twenty-one (52.5%) of the cases showed iNOS expression, 15 (37.5%) of the cases were positive for COX-2. The immunoreaction was heterogeneously distributed within the tumors. Staining intensity was different between the tumors. No correlation between iNOS and COX-2 expression was seen. There was no relationship with microvessel density. However, iNOS positive tumors developed more often distant metastases and the more malignant tumors showed a higher COX-2 expression. There was no correlation with other clinicopathological data. Approximately half of the cases expressed iNOS and COX-2. These two enzymes do not seem to be the key step in angiogenesis or carcinogenesis of pancreatic adenocarcinomas. Due to a low prevalence of COX-2 expression, chemoprevention of pancreatic carcinomas by COX-2 inhibitors can only achieve a limited success.
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v10.i13.1918