OBJECTIVE: Cyclooxygenase-2, the inducible isoform of prostaglandin H synthesis, has been implicated in the growth and progression of a various human cancer. Although COX-2 overexpression has been observed in humangliomas, the prognostic or clinical relevance of this overexpression has rarely been investigated to date. METHODS: We examined COX-2 expression by immunohistochemistry in tumor specimens from 25 patients with low- and high grade astrocytomas and correlated the grade of COX-2 expression with patients survival. RESULTS: Immunohistochemical staining results were as follows: negative staining, N=4(16%), positive staining, N=21(84%). Results of low grade astrocytoma(N=10) were as follows: negative staining, N=3(30%), weak positivestaining, N=7(70%). Anaplastic astrocytomas(N=4) as follows: negative staining, N=1(25%), weak positivestaining, N=3(75%). Glioblastomas(N=11) as follows: negative staining, N=0(0%), weak positive staining, N=5(45%), strong positive staining, N=6(55%). As a group, tumors with higher rate of cell proliferation tended to have increased expression of COX-2. The percentage of COX-2 expression were associated with a worse survival rate(p=0.0028), and the grade of astrocytic tumors(p=0.001). These findings indicate that high COX-2 expression in tumor cell is associated with clinically more aggressive gliomas, and is a strong predictor of poor survival. CONCLUSION: Our study provides evidence that COX-2 is up-regulated in the majority of high-grade gliomas and that increased COX-2 expression is a significant negative predictor of survival and selective COX-2 inhibitors may have a potential role as an adjuvant therapy of astrocytic tumors.
Astrocytoma ; Cell Proliferation ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Glioma ; Humans ; Immunohistochemistry ; Negative Staining ; Prognosis*

PURPOSE: Cyclooxygenase-2 (COX-2) expression is up-regulated in several types of human cancers and it has been suggested that COX-2 is closely inked to carcinogenesis. The objectives of this study were to investigate COX-2 expression in periampullary cancer and to evaluate the association of the clinicopathological factors with its expression. METHODS: Thirty specimens which were resected from patients with periampullary cancers (13 pancreatic adenocarcinomas, 8 common bile duct cancers, 9 ampulla of vater cancers) were investigated by immunohistochemical staining using Anti COX-2 monoclonal Ab. The 30 specimens were divided into stain-positive and stain-negative groups. The correlation between COX-2 expression and the various clinicopathological factors including the tumor size, nodal metastasis, differentiation, perineural and vascular invasion, were studied. RESULTS: COX-2 was expressed in 69% of pancreatic adenocarcinomas, 100% of common bile duct cancers and 78% of ampulla of vater cancers. However there was no significant correlation between COX-2 expression and the clinicopathological factors. CONCLUSION: COX-2 is highly expressed in periampullary cancer. Even though there was no correlation with the clinicopathological factors, the utility of the COX-2 inhibitors in preventing or treating periampullary cancer remains undetermined but warronts further investigation.
Adenocarcinoma ; Ampulla of Vater ; Carcinogenesis ; Common Bile Duct ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Humans ; Ink ; Neoplasm Metastasis

Cyclooxygenase-2 (Cox-2) is over-expressed in prostate cancer (PCa) and involved in its development and progression by facilitating inflammatory response, reducing cell apoptosis, increasing angiogenesis and damaging DNA oxidation. Selective Cox-2 inhibitors suppress PCa growth through various channels and therefore have a promising application value in the management of prostate cancer.
Apoptosis ; Cyclooxygenase 2 ; metabolism ; Cyclooxygenase 2 Inhibitors ; therapeutic use ; Humans ; Male ; Prostatic Neoplasms ; drug therapy ; metabolism

CoX-2 or prostaglandin GH synthetase-2 is an enzyme which has induction, especially in the inflamatory reactions. The inflamatory stimulations activate the CoX-2 of monocytes, macrophages, cells of synovial membrane to synthesize prostaglandin which induce the inflamatory reactions. The non- steroid anti- inflamatory drugs inhibit the CoX-2 so they have anti- inflamatory effects. However, they also inhibit CoX-1 which induce some side effects such as gastrointestinal and kidney accidents, haemorrhage and hypersensitivities. The selective CoX-2 inhibitors have some properties: long half elimination life, easier uptake by oral; the same pharmacokinetics in both elderly and children and uncommon side effects (0.1 -1% treated cases).
Anti-Inflammatory Agents, Non-Steroidal ; Pharmaceutical Preparations ; Cyclooxygenase 2 Inhibitors

As clinical study showed that COX-2 is strengthened in the angiogenesis, apoptosis, invasive and increasing immunization in the process of tumor progress. The first result of use inhibitor COX-2 has potential in prevention and treatment of tumor. Use COX-2 in progress of prostate cancer as metastasis tumor and be low isolated. Use COX-2 in bladder tumor without response with BCG and after cut off bladder. Use COX-2 in metastasis kidney tumor or have high risk in Von Hippel-Lindau
Urologic Neoplasms ; Cyclooxygenase 2 Inhibitors ; Hippel-Lindau Disease ; Therapeutics ;

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to treat pain and inflammation. There are two kinds of NSAID classified according to the selectivity of COX-2 inhibition: non-selective NSAIDs and cyclooxygenase (COX)-2 inhibitors. Non-selective NSAIDs have a high incidence of gastrointestinal and bleeding-associated adverse events, while COX-2 inhibitors are safer in terms of these events. However, COX-2 inhibitors are thought to cause increased cardiovascular events. The COX-2 inhibitors rofecoxib and valdecoxib were withdrawn from the market over safety concerns. Three COX-2 inhibitors are now available in South Korea after the recent approval of etoricoxib and polmacoxib for osteoarthritis patients. After reviewing the history of and recent studies about the safety of COX-2 inhibitors, physicians should find new uses for old drugs.
Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 Inhibitors* ; Cyclooxygenase Inhibitors ; Humans ; Incidence ; Inflammation ; Korea ; Osteoarthritis ; Prostaglandin-Endoperoxide Synthases

OBJECTIVE: In vitro studies have revealed that treatment of various human cancer cell lines with specific cyclooxygenase 2 (COX-2) inhibitors induces apoptotic cell death. The goal of this article is to investigate the benefits of combining COX-2 inhibitors with existing treatment modalities in the management of ovarian cancer. METHODS: In this study we sought to determine the effects of combining paclitaxel and the COX-2 inhibitor celecoxib on apoptosis of epithelial ovarian cancer (EOC) cells. SK-OV-3 cells were exposed to increasing concentrations of paclitaxel (10(-7) M, 10(-6) M and 10(-5) M) and celecoxib (10(-8) M, 10(-7) M, 10(-6) M, 10(-5) M and 10(-4) M) as well as a combination of both drugs. The activity of apoptosis was evaluated by the morphologic examination and the MTT assay. The pattern of apoptosis was also assessed by the caspase-3 activity and the fraction of cleaved PARP (poly ADP-ribose polymerase) protein. RESULTS: Single application of both drugs could significantly increase the rate of apoptosis after 24 hours of continuous exposure. But concomitant treatment of SK-OV-3 EOC cell line with paclitaxel and celecoxib resulted in marked impairment of paclitaxel-induced apoptosis. The pattern of apoptosis induced by paclitaxel on SK-OV-3 EOC cell line was caspase-3 independent. CONCLUSION: Combining COX-2 inhibitors and paclitaxel does not have an additive or synergistic tumoricidal effect. On the contrary, celecoxib treatment markedly inhibited the apoptotic effects of paclitaxel in SK-OV-3 EOC cell line.
Adenosine Diphosphate Ribose ; Apoptosis* ; Caspase 3 ; Cell Death ; Cell Line* ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Humans ; Ovarian Neoplasms* ; Paclitaxel ; Celecoxib

PURPOSE: This study was performed to investigate the effects of intravesical instillation of cyclooxygenase-2 (COX-2) inhibitors on the cyclophosphamide-induced overactive bladder. MATERIALS AND METHODS: The 40 Sprague-Dawley rats were divided into 3 groups; the control group, the overactive group, and the COX-2 inhibitor treated group. Cystometrograms (CMG) were performed and the contraction interval, inter-contraction interval, contraction time and contraction pressure were measured. After CMG, the bladders of each group were dissected out, and weighed. RESULTS: On CMG, the contraction interval and inter-contraction interval for the overactive group were significantly decreased compared with the control group. After treatment with COX-2 inhibitor, the contraction interval and inter-contraction interval were significantly increased compared with the overactive group (p<0.05). The contraction time in the overactive group was significantly increased compared with the control group, and it was also decreased in the COX-2 inhibitor treated group compared with the overactive group (p<0.05). The contraction pressure in the overactive group and the COX-2 inhibitor treated group were significantly increased compared with the control group. There were no significant differences between the overactive and COX-2 inhibitor treated groups. The bladder weights of the overactive and COX-2 inhibitor treated groups were significantly increased compared with the control group (p<0.05). CONCLUSIONS: Intravesical instillation of COX-2 inhibitor can suppress cyclophosphamide-induced detrusor overactivity. Therefore, intravesical instillation of COX-2 inhibitor may be considered as a possible treatment for the overactive bladder.
Administration, Intravesical* ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Cyclophosphamide ; Rats, Sprague-Dawley ; Urinary Bladder ; Urinary Bladder, Overactive* ; Weights and Measures

PURPOSE: This study was performed to investigate the effects of intravesical instillation of cyclooxygenase-2 (COX-2) inhibitors on the cyclophosphamide-induced overactive bladder. MATERIALS AND METHODS: The 40 Sprague-Dawley rats were divided into 3 groups; the control group, the overactive group, and the COX-2 inhibitor treated group. Cystometrograms (CMG) were performed and the contraction interval, inter-contraction interval, contraction time and contraction pressure were measured. After CMG, the bladders of each group were dissected out, and weighed. RESULTS: On CMG, the contraction interval and inter-contraction interval for the overactive group were significantly decreased compared with the control group. After treatment with COX-2 inhibitor, the contraction interval and inter-contraction interval were significantly increased compared with the overactive group (p<0.05). The contraction time in the overactive group was significantly increased compared with the control group, and it was also decreased in the COX-2 inhibitor treated group compared with the overactive group (p<0.05). The contraction pressure in the overactive group and the COX-2 inhibitor treated group were significantly increased compared with the control group. There were no significant differences between the overactive and COX-2 inhibitor treated groups. The bladder weights of the overactive and COX-2 inhibitor treated groups were significantly increased compared with the control group (p<0.05). CONCLUSIONS: Intravesical instillation of COX-2 inhibitor can suppress cyclophosphamide-induced detrusor overactivity. Therefore, intravesical instillation of COX-2 inhibitor may be considered as a possible treatment for the overactive bladder.
Administration, Intravesical* ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase 2* ; Cyclophosphamide ; Rats, Sprague-Dawley ; Urinary Bladder ; Urinary Bladder, Overactive* ; Weights and Measures

The cyclooxygenase (COX) is a key enzyme in the coversion of arachidonic acid to prostaglandins. COX-1 is constitutively expressed and is a critical housekeeping gene, whereas COX-2 is rapidly upregulated by growth factors and cytokines and thus responsible for inflammation. COX-2 is frequently overexpressed in colonic adenoma and carcinoma. Specific inhibitors of COX-2 have been shown to induce apoptosis in tumor cells and to inhibit tumor growth in animal models and in humans. Long-standing IBD patients have increased risk of developing colorectal cancer compared to general population. IBD-associated colorectal carcinogenesis is probably promoted by chronic inflammation and closely related to COX-2. In a recent study, powerful chemopreventive ability of selective COX-2 inhibitor was observed in colitis-related colon carcinogenesis in mouse model. But it was reported that even selective COX inhibitors aggravated the DSS-induced colonic inflammation. It is assumed that endogenous PGs are involved in the mucosal defense against DSS-induced colonic ulcerations which are produced by COX-1 at early phase and by COX-2 at late phase. Long-term use of COX-2 inhibitors for the chemoprevention of colitic cancer is needed to define their mechanism of action, that reduce side effects and have specific tumor target.
Animals ; Colitis, Ulcerative/*drug therapy ; Colonic Neoplasms/diagnosis ; Cyclooxygenase 1/metabolism ; Cyclooxygenase 2/metabolism ; Cyclooxygenase 2 Inhibitors/pharmacology/*therapeutic use ; Humans ; Mice ; Models, Animal