Correlation between cyclooxygenase-2, proliferative activity, and mucin phenotype in human advanced gastric cancer.

BACKGROUND: Recent studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of gastrointestinal cancer, and that cyclooxygenase-2 (COX-2) may be a target enzyme for the prevention or regression of cancer by the use of NSAIDs. Mucin histochemistry has made possible a clear distinction between the differentiated characteristics of gastrointestinal epithelial cells, and the possibility that phenotypic shifts from gastric- to intestinal-type in gastric carcinoma progression has been suggested. To evaluate the role of COX-2 in gastric cancer progression, we immunohistochemically investigated COX-2 expression, and examined its relationship to proliferative activity, mucin phenotype, and clinicopathological parameters in human advanced gastric carcinomas. METHODS: Forty-five surgical specimens of advanced gastric carcinomas (invaded the muscularis propria or subserosa) were examined. Immunohistochemical staining was performed with monoclonal antibodies against COX-2, Ki-67, CD10 (brush border), MUC-2 (goblet-cell mucin), MUC-5AC (gastric foveolar mucin), and MUC-6 (pyloric mucin). COX-2 expression was scored by the percentage of COX-2-positive neoplastic cells, and proliferative activity was assessed by the Ki-67 labeling index at the deepest area of invasion. The mucin phenotype of the carcinomas was classified into three categories; gastric, intestinal, and unclassified. RESULTS: COX-2 staining was restricted to the cytoplasm, not only in cancer cells but also in intestinal metaplasia and some inflammatory cells and COX-2 expression in cancer cells varied greatly, but the staining in some samples was preferentially found at the invasive front. COX-2 positivity was found to correlate with Ki-67 labeling. The mean COX-2 scores were 2.29%, 2.71%, and 2.75%; and the Ki-67 labeling indices were 23.6%, 40.6%, and 56.5%, in gastric-, intestinal-, and unclassified- type carcinomas, respectively. CONCLUSIONS: A close relationship between COX-2 expression and proliferative activity was confirmed in the deepest areas of advanced gastric carcinoma, and the proliferative activity increased from gastric- to intestinal- and to unclassified- type gastric carcinoma, suggesting a role for COX-2 expression and differences in biological behavior according to mucin phenotype expression during gastric cancer progression.

A case of pseudotumorous pancreatitis that presented unique pancreatoscopic findings with the peroral electronic pancreatoscope.

A 49-year-old man was admitted to Hospital of Kyoto Prefectural University of Medicine complaining of epigastralgia and jaundice. There was a tumor (approximately 30 mm) in the pancreatic head on ultrasound, computed tomography and magnetic resonance imaging. Endoscopic retrograde cholangiopancreatography revealed a stenosis of the main pancreatic duct in the head of the pancreas. Pancreatoscopy with the peroral electronic pancreatoscope (PEPS) was performed to differentiate between pseudotumorous pancreatitis (PTP) and pancreatic carcinoma. The PEPS showed non-erosive erythematous mucosa around the stenosis and this unique finding was different from that of pancreatic carcinoma. Pylorus-preserving pancreatoduodenectomy was performed under the possible diagnosis of carcinoma. As a result, the diagnosis of PTP was confirmed histopathologically. At present, the diagnosis of PTP is difficult because of similar findings with carcinoma in various imaging procedures. However, we consider that detailed observation and accurate morphologic assessment of the main pancreatic duct with the PEPS has the possibility of differentiating PTP from pancreatic carcinoma.