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Abstract
Objectives. The inescapable relationship between chronic inflammation and carcinogenesis has long been established. Our objective was to investigate COX-2 and NF-κB immunohistochemical expression in a large series of normal epithelium and bladder carcinomas. Methods. Immunohistochemical methodology was performed on formalin-fixed, paraffin-embedded sections from urinary bladder carcinomas of 140 patients (94 males and 46 females with bladder carcinomas). Results. COX-2 expression is increased in the cytoplasm of bladder cells, during loss of cell differentiation (r s = 0.61, P-value < .001) and in muscle invasive carcinomas (P-value < .001). A strong positive association between tumor grade and nuclear expression of NFκB has been established. A positive correlation between COX-2 and nuclear NFκB immunoreactivity was observed. Conclusions. The possible coordinated upregulation of NFκB and COX-2, during bladder carcinogenesis, indicates that agents inhibitors of these two molecules may represent a possible new treatment strategy, by virtue of their role in bladder carcinogenesis.
Highlights
Urothelial carcinoma (UC) of the urinary bladder is the third most common cancer in men and the 15th most common cancer in women
To better understand the importance of chronic inflammation in bladder cancer pathogenesis and progression, we investigated COX-2 and Nuclear Factor-κB (NF-κB) p65 immunohistochemical expression in a large series of normal epithelium and bladder carcinomas, and we correlated those findings with cancer cell differentiation, tumor grade and stage, and clinical-pathologic features of bladder cancer patients
COX-2 expression was positively correlated with T-tumor category and in muscle invasive carcinomas (Figure 2(b))
Summary
Urothelial carcinoma (UC) of the urinary bladder is the third most common cancer in men and the 15th most common cancer in women. The more frequent form of this carcinoma is either non-invasive or superficially invasive disease, which is usually curable, but demonstrates a challenge to the clinician because of its recurrent nature. More effective therapies are needed to prevent recurrence of superficial UC and to inhibit progression of noninvasive tumors to invasive carcinomas [2]. Chronic inflammation is recognized as crucial in the pathogenesis of a variety of diseases, such as arthritis, diabetes, atherosclerosis, Alzheimer’s disease, and cancer development, including bladder cancer [3]. To better understand the importance of chronic inflammation in bladder cancer pathogenesis and progression, we investigated COX-2 and NF-κB p65 immunohistochemical expression in a large series of normal epithelium and bladder carcinomas, and we correlated those findings with cancer cell differentiation, tumor grade and stage, and clinical-pathologic features of bladder cancer patients
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