Results from epidemiological studies indicate that long-term intake of non-steroidal anti-inflammatory drugs, which inhibit cyclooxygenase (COX) enzymes involved in prostaglandin biosynthesis, reduces the risk of several forms of human malignancies. Expression of COX-2 in tumors is known to be associated with enhanced angiogenesis, suppression of host immunity, and tumor invasion. Genetic or pharmacological inhibition of COX-2 has been shown to protect against experimentally-induced carcinogenesis and to reduce the growth of xenografted tumors in animal models. A number of studies also revealed that COX-2 inhibition suppresses proliferation, metastatic potential, and other functions of cancer cell lines. Thus, it is conceivable that targeted inhibition of abnormally or improperly elevated COX-2 provides one of the most effective and promising strategies for cancer therapy. In this review, the involvement of COX-2 in the tumorigenesis of oral cancers and the potential mechanisms of tumor suppressive effects of COX-2 inhibition are discussed.

Results from epidemiological studies indicate that long-term intake of non-steroidal anti-inflammatory drugs, which inhibit cyclooxygenase (COX) enzymes involved in prostaglandin biosynthesis, reduces the risk of several forms of human malignancies. Expression of COX-2 in tumors is known to be associated with enhanced angiogenesis, suppression of host immunity, and tumor invasion. Genetic or pharmacological inhibition of COX-2 has been shown to protect against experimentally-induced carcinogenesis and to reduce the growth of xenografted tumors in animal models. A number of studies also revealed that COX-2 inhibition suppresses proliferation, metastatic potential, and other functions of cancer cell lines. Thus, it is conceivable that targeted inhibition of abnormally or improperly elevated COX-2 provides one of the most effective and promising strategies for cancer therapy. In this review, the involvement of COX-2 in the tumorigenesis of oral cancers and the potential mechanisms of tumor suppressive effects of COX-2 inhibition are discussed.

A case of tricuspid regurgitation due to nonpenetrating chest trauma was presented. A 58-year-old man who had an episcde of a traffic accident 18 years ago was admitted because of the edema of the lower extremities and easy fatigability. On physical examination, engorgement of the jugular vein, enlagement of the liver and the slight edema of the lower extremities were observed. Systolic regurgitant murmur with Rivero-Carvallo sign was audible. Chest X-ray film revealed marked cardiomegaly and electrocardiogram presented atial fibrillation and complete right bundle branch block. Two-dimentional echocardiography revealed marked dilatation of the right atrium and ventricle, and systolic exertion of anterior and posterior leaflets of tricuspid valve. On cardiac catheterization, right atrial v wave was 23mm Hg. At operation, the pericardium was adheded to the epicardium, and the chorda tendae of the anterior and posterior leaflet were ruptured. Tricuspid valve replacement with 33mm Carpentier-Edwards pericardial prosthetic valve was performed without any complications. To the best of our knowledge, this is the 19th operated case of traumatic tricuspid regurgitation in Japan.

We report a case of cholesterol crystal embolism (CCE) after endovascular aortic repair for abdominal aortic aneurysm (AAA). A 68-year-old man with AAA underwent endovascular aortic repair. He complained of left lower abdominal pain after the operation. Abdominal CT showed renal infarction on postoperative day 10. Renal dysfunction developed after postoperative day 17. A biopsy of the renal infarct lesion demonstrated characteristic cholesterol clefts in the small arteries. We diagnosed CCE. Steroid therapy was administered and the patient's condition improved remarkably. Diagnosis of CCE is difficult and its prognosis still remains poor. Therefore, we should keep this unusual complication in mind.

Immunoglobulin G4 (IgG4)-related disease can occur in various organs, most of which comprise glandular or ductal tissue. We report a case of IgG4-related disease which occurred in a cardiovascular lesion. A 69-year-old man was found to have a tumorous lesion around the coronary artery. Open chest biopsy showed the diffuse lymphoplasmacytic infiltration, occasional eosinophils and numerous IgG4-positive plasma cells within the lesions. The serum concentration of IgG4 in the postoperative period was 1,080 mg/dl (reference range, <135). We diagnosed IgG4-related periarteritis manifesting as a tumor around the coronary artery. This case suggests that IgG4-related disease can occur around the coronary artery and manifest as a periarterial mass lesion.