Cyclooxygenase-2: a target for the prevention and treatment of breast cancer.

2001 ◽  
pp. 97-114 ◽  
Author(s):  
L R Howe ◽  
K Subbaramaiah ◽  
A M Brown ◽  
A J Dannenberg
Keyword(s):  
Breast Cancer ◽  
Mammary Tumorigenesis ◽  
Cyclooxygenase 2 ◽  
Cancer Data ◽  
Prostaglandin Synthase ◽  
Tumour Formation ◽  
Prevention And Treatment ◽  
Cox 2 ◽  
Cox 2 Inhibitors

Cyclooxygenase-2 (COX-2), an inducible prostaglandin synthase, is normally expressed in parts of the kidney and brain. Aberrant COX-2 expression was first reported in colorectal carcinomas and adenomas, and has now been detected in various human cancers, including those of the breast. Strikingly, COX-2 overexpression in murine mammary gland is sufficient to cause tumour formation. To date, the role of COX-2 in tumorigenesis has been most intensively studied in the colon. Thus, the relationship between COX-2 and neoplasia can best be illustrated with reference to intestinal tumorigenesis. Here we consider the potential utility of selective COX-2 inhibitors for the prevention and treatment of breast cancer. Data for cancers of the colon and breast are compared where possible. In addition, the mechanisms by which COX-2 is upregulated in cancers and contributes to tumorigenesis are discussed. Importantly, several recent studies of mammary tumorigenesis in animal models have found selective COX-2 inhibitors to be effective in the prevention and treatment of breast cancer. Clinical trials will be needed to determine whether COX-2 inhibition represents a useful approach to preventing or treating human breast cancer.

scholarly journals Selective cyclooxygenase-2 (COX-2) inhibitors and breast cancer risk

The Breast ◽  
2011 ◽  
Vol 20 (1) ◽  
pp. 66-70 ◽  
Author(s):  
Varun Ashok ◽  
Chiranjeev Dash ◽  
Thomas E. Rohan ◽  
J. Michael Sprafka ◽  
Paul D. Terry
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Cyclooxygenase 2 ◽  
Cox 2 ◽  
Cox 2 Inhibitors

scholarly journals Role of Cyclooxygenase 2 (COX-2) in Prognosis of Breast Cancer

2014 ◽  
Vol 5 (1) ◽  
pp. 59-65 ◽  
Author(s):  
Debarshi Jana ◽  
Diptendra Kumar Sarkar ◽  
Suvro Ganguly ◽  
Shilpi Saha ◽  
Gaurisankar Sa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cyclooxygenase 2 ◽  
Cox 2

COX-2 inhibitors and genetic background reduce mammary tumorigenesis in cyclooxygenase-2 transgenic mice

2005 ◽  
Vol 76 (1-4) ◽  
pp. 86-94 ◽  
Author(s):  
Kirsi Narko ◽  
Ben Zweifel ◽  
Ovidiu Trifan ◽  
Ari Ristimäki ◽  
Timothy F. Lane ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Genetic Background ◽  
Mammary Tumorigenesis ◽  
Cyclooxygenase 2 ◽  
Cox 2 ◽  
Cox 2 Inhibitors

Inhibition of cyclooxygenase-2 ameliorates the severity of pancreatitis and associated lung injury

2002 ◽  
Vol 283 (5) ◽  
pp. G1166-G1174 ◽  
Author(s):  
Albert M. Song ◽  
Lakshmi Bhagat ◽  
Vijay P. Singh ◽  
Gijs G. D. Van Acker ◽  
Michael L. Steer ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Lung Injury ◽  
Lavage Fluid ◽  
Cyclooxygenase 2 ◽  
Neutrophil Sequestration ◽  
Acinar Cell Necrosis ◽  
Cox 2 ◽  
Proinflammatory Role ◽  
Cox 2 Inhibitors

Cyclooxygenase-2 (COX-2), a widely distributed enzyme, plays an important role in inflammation. We have studied the role of COX-2 in acute pancreatitis and pancreatitis-associated lung injury using both the pharmacological inhibition of COX-2 and genetic deletion of COX-2. Pancreatitis was induced in mice by 12 hourly injections of cerulein. The severity of pancreatitis was assessed by measuring serum amylase, pancreatic trypsin activity, intrapancreatic sequestration of neutrophils, and acinar cell necrosis. The severity of lung injury was evaluated by measuring lactate dehydrogenase levels in the bronchoalveolar lavage fluid and by quantitating neutrophil sequestration in the lung. In both the pharmacologically inhibited and genetically altered mice, the severity of pancreatitis and pancreatitis-associated lung injury was reduced compared with the noninhibited strains of COX-2-sufficient mice. This reduction in injury indicates that COX-2 plays an important proinflammatory role in pancreatitis and its associated lung injury. Our findings support the concept that COX-2 inhibitors may play a beneficial role in the prevention of acute pancreatitis or in the reduction of its severity.

RELATIVE ROLE OF CYCLOOXYGENASE-2 (COX-2) INHIBITORS AND LIPOXYGENASE (LOX) INHIBITORS IN AGING INDUCED DEMENTIA AND OXIDATIVE DAMAGE

2005 ◽  
Vol 12 (02) ◽  
pp. 6-11 ◽  
Author(s):  
Mahendra Bishnoi ◽  
Chandrashekhar S Patii ◽  
Anil Kumar ◽  
Shrinivas K Kulkarni
Keyword(s):  
Oxidative Damage ◽  
Cyclooxygenase 2 ◽  
Relative Role ◽  
Cox 2 ◽  
Lox Inhibitors ◽  
Cox 2 Inhibitors

scholarly journals Cyclooxygenase-2 (COX-2) inhibitors: future therapeutic strategies for epilepsy management

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Chitra Rawat ◽  
Samiksha Kukal ◽  
Ujjwal Ranjan Dahiya ◽  
Ritushree Kukreti
Keyword(s):  
Underlying Mechanism ◽  
Cyclooxygenase 2 ◽  
World Population ◽  
Clinical Settings ◽  
Dose Time ◽  
Proinflammatory Mediators ◽  
Pathophysiological Role ◽  
Cox 2 ◽  
Cox 2 Inhibitors

Abstract Epilepsy, a common multifactorial neurological disease, affects about 69 million people worldwide constituting nearly 1% of the world population. Despite decades of extensive research on understanding its underlying mechanism and developing the pharmacological treatment, very little is known about the biological alterations leading to epileptogenesis. Due to this gap, the currently available antiepileptic drug therapy is symptomatic in nature and is ineffective in 30% of the cases. Mounting evidences revealed the pathophysiological role of neuroinflammation in epilepsy which has shifted the focus of epilepsy researchers towards the development of neuroinflammation-targeted therapeutics for epilepsy management. Markedly increased expression of key inflammatory mediators in the brain and blood-brain barrier may affect neuronal function and excitability and thus may increase seizure susceptibility in preclinical and clinical settings. Cyclooxygenase-2 (COX-2), an enzyme synthesizing the proinflammatory mediators, prostaglandins, has widely been reported to be induced during seizures and is considered to be a potential neurotherapeutic target for epilepsy management. However, the efficacy of such therapy involving COX-2 inhibition depends on various factors viz., therapeutic dose, time of administration, treatment duration, and selectivity of COX-2 inhibitors. This article reviews the preclinical and clinical evidences supporting the role of COX-2 in seizure-associated neuroinflammation in epilepsy and the potential clinical use of COX-2 inhibitors as a future strategy for epilepsy treatment.

scholarly journals Chronic Low-Level Lead Exposure Increases Mesenteric Vascular Reactivity: Role of Cyclooxygenase-2-Derived Prostanoids

2021 ◽  
Vol 11 ◽  
Author(s):  
Maylla Ronacher Simões ◽  
Bruna Fernandes Azevedo ◽  
María Jesús Alonso ◽  
Mercedes Salaices ◽  
Dalton Valentim Vassallo
Keyword(s):  
Lead Exposure ◽  
Vascular Reactivity ◽  
Cyclooxygenase 2 ◽  
Resistance Arteries ◽  
Induced Hypertension ◽  
Pb Exposure ◽  
Cox 2 ◽  
Underlying Mechanisms ◽  
Cox 2 Inhibitors

Lead (Pb) exposure causes hazardous effects as hypertension and other cardiovascular diseases. We evaluated whether chronic Pb exposure alters the peripheral vascular resistance measuring the vascular reactivity of mesenteric resistance arteries in rats to identify the underlying mechanisms that are associated to the development of Pb-induced hypertension. Mesenteric resistance arteries from lead-treated and untreated Wistar rats (1st dose: 10 μg/100 g; subsequent doses: 0.125 μg/100 g, intramuscular, 30 days) were used. Contractile responses to phenylephrine increased, while acetylcholine and sodium nitroprusside-induced relaxation was not affected by lead treatment. Endothelium removal and inhibition of NO synthase by L-NAME similarly enhanced the response to phenylephrine in untreated and lead-treated rats. The antioxidants apocynin and superoxide dismutase (SOD) did not affect vasoconstriction in either group. The vascular expression of cyclooxygenase-2 (COX-2) protein increased after lead exposure. The respective non-specific or specific COX-2 inhibitors indomethacin and NS398 reduced more strongly the response to phenylephrine in treated rats. Antagonists of EP1 (SC19220), TP (SQ29548), IP (CAY10441) and angiotensin II type 1 (losartan) receptors reduced vasoconstriction only in treated rats. These conclusions present further evidence that lead, even in small concentration, produces cardiovascular hazards being an environmental contaminant that account for lead-induced hypertension.

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