The intravesical application of dilute HCl in rats results in a histologic appearance which mimics that seen in humans with interstitial cystitis. The appearance of detrusor mastocytosis and eosinophilia was accompanied by a relative decrease in the expression of gamma- and a relative increase in alpha-smooth muscle isoactin gene expression. This pattern of smooth muscle isoactin expression is consistent with a more immature and possibly synthetic smooth muscle phenotype, which may be responsible for the clinical presentation of those with IC. Northern blot analysis of bladder smooth muscle cells may serve as an effective marker for the development of interstitial cystitis in humans.

MITOSTATIN, a novel putative tumor suppressor gene induced by decorin overexpression, is expressed in most normal human tissues but is markedly down-regulated in advanced stages of mammary and bladder carcinomas. Mitostatin negatively affects cell growth, induces cell death and regulates the expression and activation levels of Hsp27. In this study, we demonstrated that ectopic expression of Mitostatin in PC3, DU145, and LNCaP prostate cancer cells not only induced a significant reduction in cell growth, but also inhibited migration and invasion. Moreover, Mitostatin inhibited colony formation in soft-agar of PC3 and LNCaP cells as well as tumorigenicity of LNCaP cells in nude mice. Conversely, targeting endogenous Mitostatin by siRNA and anti-sense strategies in PC3 and DU145 prostate cancer cells enhanced the malignant phenotype in both cell lines. In agreement of these anti-oncogenic roles, we discovered that Mitostatin was absent in ∼35% (n = 124) of prostate tumor samples and its overall reduction was associated with advanced cancer stages. Collectively, our findings indicate that MITOSTATIN may acts as a tumor suppressor gene in prostate cancer and provide a novel cellular and molecular mechanism to be further exploited and deciphered in our understanding of prostate cancer progression.

No abstract

No abstract

No abstract

The mucin lining of the bladder is thought to serve as a primary defense mechanism against bacterial colonization, and has recently been implicated in the urothelial resistance to carcinogenic insult. We have isolated a unique glycoprotein fraction (GP1) of this lining from the normal rabbit bladder which may have a function in preventing bacterial adherence and colonization in the urinary tract. This glycoprotein has been shown to bind to a wide range of uropathic bacteria. The present study examines changes in the bladder's antibacterial defense mechanisms as measured by GP1 expression in the neoplastic state. Using an anti-GP1 serum, immunohistochemical staining was performed on 20 paraffinized and fresh frozen transitional cell carcinomas ranging from low grade, superficial tumors to high grade, invasive tumors. The presence of GP1 was seen throughout the mucosal layer in normal specimens with increased amounts noted towards the mucosal surface. Progressively decreased expression was noted with increasing grades of all transitional carcinoma specimens. Mucosal field changes in GP1 expression were not noted in any of the patients. Intestinal mucosal controls failed to detect the presence of GP1. These studies suggest that the expression of GP1 decreases with tumor dedifferentiation and that bladder tumorogenesis may serve a role in handicapping the bladder's primary antibacterial defense mechanism.

No abstract

The intravesical application of dilute HCl in rats results in a histologic appearance which mimics that seen in humans with interstitial cystitis. The appearance of detrusor mastocytosis and eosinophilia was accompanied by a relative decrease in the expression of gamma- and a relative increase in alpha-smooth muscle isoactin gene expression. This pattern of smooth muscle isoactin expression is consistent with a more immature and possibly synthetic smooth muscle phenotype, which may be responsible for the clinical presentation of those with IC. Northern blot analysis of bladder smooth muscle cells may serve as an effective marker for the development of interstitial cystitis in humans.