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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. [ABSTRACT FROM AUTHOR]

Purpose: the peroxisome proliferator-activated receptor γ (PPARγ), known to play a key role in homeostatic biological pathways, is also implicated in the process of carcinogenesis. Ligands for PPARγ and its heterodimeric partner, retinoid-X receptor (RXR), have exhibited anticancer effects both in vitro and in vivo. Unexpectedly, some studies suggested that PPARγ ligands may stimulate cancer formation. This study aimed to estimate the signaling of PPARγ-RXRα heterodimer in bladder urothelial carcinomas (BUC)., Methods: we studied PPARγ and RXRα expression in specimens obtained from 97 patients with BUC of various grades and stages using immunohistochemistry., Results: PPARγ expression was significantly downregulated with BUC stage and grade progression, and the dynamics of this phenomenon was significantly influenced by RXRα's level of expression., Conclusion: the positive association of PPARγ expression in BUC with more differentiated, non-invasive tumors is strengthened by the presence of RXRα. This knowledge could probably be of use in the development of new chemotherapeutic agents.

Continuous exposure of newborn mice of a single, highly inbred strain to 100% oxygen at normal atmospheric pressure for up to 6 weeks resulted in a progressive evolution of pulmonary changes which consisted of dense fibrous tissue deposition, chronic bronchitis and bronchiolitis, and emphysema. Survival of the experimental animals decreased with the duration of exposure, and it was 18% after the sixth week. While the pulmonary changes were evolving, lung growth was markedly inhibited in the experimental animals, whereas lung weight increased significantly. The present study indicates that in contrast to the adult mouse, survival of a substantial percentage of newborn mice for at least 6 weeks is possible, but it is associated with severe changes in pulmonary structure that doubtlessly lead to serious derangement of cardiopulmonary functions.