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Objectives: Functional E-cadherin adhesion complexes are necessary to maintain the normal differentiated phenotype in bladder epithelial cells and dysfunction of molecules in this complex is associated with an invasive phenotype. Moreover, loss of functioning of E-cadherin and/or a-catenin in cancer cells is associated with a poor prognosis for bladder cancer patients. Clearly, other adhesion molecules are also involved in the process of invasion and/or metastasis. For example the expression of activated leukocyte cell adhesion molecule, ALCAM, an adhesion molecule belonging to the immunoglobulin superfamily, appeared to be correlated with malignant potential in human melanoma.Methods: The expression of ALCAM in human bladder cancer specimens was studied by immunohistochemistry and correlated with E-cadherin and a-catenin expression.Results: In normal bladder tissue, only the umbrella cells showed positive membrane staining of ALCAM. In 19 out of 52 bladder cancer specimens, we found ALCAM staining, particularly in those areas that showed aberrant expression of a-catenin and E-cadherin.Conclusions: There was a correlation between ALCAM expression in tumor cells and stage and grade, i.e. T a21 :0/15, . T 1 : 19/37 (36.5%), G1: 0/5, G2: 2/14 (14.3%) and G3: 17/33 (51.5%) (T a21 : . T 1 , p ¼ 0:0002; G1:G2:G3, p ¼ 0:0108). Moreover, positive ALCAM expression was strongly associated with a poor prognosis for bladder cancer patients. Multivariate analysis showed that ALCAM immunohistochemistry had additional prognostic value over pathological stage. Furthermore, it provides better prediction of prognosis when compared to grade and aberrant E-cadherin or a-catenin staining.

A 67-year-old man was treated with maintenance intravesical BCG for superficial bladder cancer. As a culture-proven complication of this therapy, he developed general malaise, high fever, granulomatous hepatitis and a mycotic aneurysm in his left knee. All complications were treated successfully with antituberculous therapy. No vascular surgery was necessary. This case report again stresses the necessity to recognise complications of BCG treatment and to start adequate therapy as soon as possible.

OBJECTIVE To analyse and compare the concentration of plasminogen activator (PA), urokinase‐type PA (uPA), tissue‐type PA (tPA), PA inhibitor (PAI)‐1 and PAI‐2, and the complexes uPA‐PAI‐1 and tPA‐PAI‐1 and calculated uPA and tPA uncomplexed with PAI‐1 (‘free’) in urothelial cell carcinoma and matched benign urothelium, and in renal cell carcinoma (RCC) and matched benign renal tissue. PATIENTS AND METHODS Tissue samples were obtained during cystectomy (33 patients) and nephrectomy (55), and specific enzyme‐linked immunosorbent assays were used to assess the PA components in extracts of these tissues. RESULTS Tissue levels of uPA‐PAI‐1 and tPA‐PAI‐1, but also PAI‐1 itself, were greater in tumorous bladder and kidney tissue than in matched normal tissue (by 1.5–7.8 times). Free tPA was clearly lower in tumour tissue (by 0–0.12‐fold). In bladder cancer, but not in RCC, levels of uPA (15.8‐fold) and free uPA (16.4‐fold) were greater in tumour tissue. Free uPA levels were less in RCC (0.41‐fold). For both normal bladder and kidney tissue, there was no clear correlation between uPA‐PAI‐1 complex and either component. However, the formation of tPA‐PAI‐1 complexes in normal bladder and kidney tissue was primarily determined by PAI‐1. Interestingly, in tumour tissues there was a strong, significant correlation between complex levels and both components. CONCLUSION RCC and bladder cancer show distinct profiles of components of the PA system. This study provides a basis for further studies into both the (patho)physiological role of the PA system in these tumours, and into a possible relation with tumour progression and prognosis, and as target for therapy.