Related Experiment Video
Updated: Mar 28, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Expression of Cyclooxygenase-2 Protein in Gastric Carcinogenesis
Purpose:
The increased expression of cyclooxygenase (COX)-2 has been implicated in the development and progression of human cancers. We investigated COX-2 expression in normal, gastric adenomas and adenocarcinomas.
Materials And Methods:
COX-2 protein was assayed in gastrectomy and biopsy specimens, from 68 gastric adenocarcinomas, 40 gastric adenomas and 35 normal gastric tissues, by immunohistochemistry, and 32 specimens of normal and adenocarcinomas by western blot analysis. Correlation between COX-2 expression and various clinicopathological factors were studied in the gastric adenocarcinoma.
Results:
COX-2 protein expression in epithelial cells was increased in 6/40 (15%) of the adenomas and 55/68 (80.9 %) of the adenocarcinomas, while normal mucosa was not expressed. COX-2 expression was increased in differ-entiated gastric carcinomas compared with those in the undifferentiated group (p<0.05). The expression of COX-2 protein was unrelated to tumor size, depth of tumor invasion and the presence of lymphatic or vascular invasions. Western blot analysis showed the enhanced expression of the COX-2 protein (23 out of 32)(71%) in gastric carcinomas compared to that of normal gastric mucosal epithelium.
Conclusion:
The above results indicated that the expression of COX-2 protein occurs in dysplastic epithelium and gastric carcinomas, which suggests COX-2 expression may contribute to tumor formation.
More Related Videos
Related Concept Videos
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

