Endothelial cell proliferation and vascular patterns in urothelial carcinoma.

INTRODUCTION: The bladder cancer has some characteristics: the sixth most incident neoplasm in the United States, the majority of diagnosed cases in those 55 years of age and older, four times more common in man than women, a reduced five-year survival rate in case of metastatic disease. Despite the beneficial effects of the combination therapy and immunotherapy, the low response rate and drug resistance were reported. The main goal of this work was evaluation of the endothelial cell proliferation from urothelial carcinomas. PATIENTS, MATERIALS AND METHODS: Fifty-two cases of T2-T4 infiltrative bladder tumors, aged between 46 and 78 years, were investigated. Morphological, simple and cluster of differentiation 31 (CD31)∕Ki67, CD31∕smooth muscle actin (SMA) double immunostaining were performed. RESULTS: In all the analyzed infiltrative bladder tumors, three types of vessels were noticed: immature, intermediate and mature. In the central part of the tumor area, the following distribution of vessel types was noticed: immature (62.25%), intermediate (35.1%), and mature vessels (2.65%). In the peripheral tumor area, the intermediate vessels increase numerically, up to 54% and the mature ones, up to 18.6%. The peritumoral area was characterized by the absence of immature vessels and the presence of intermediate and mature ones only. It was found the presence of endothelial cell nuclei stained for Ki67 only for immature and intermediate vessels, and never for mature ones. CONCLUSIONS: The vascular patterns may contribute to a better stratification of the patient subgroups and antiangiogenic treatment algorithms.

Chloride Intracellular Channel Protein 1 (CLIC1) Ιs Over-expressed in Muscle Invasive Urinary Bladder Cancer.

BACKGROUND/AIM: Invasive bladder cancer mortality remains high despite progresses made in early diagnosis and surgical procedures. Thus, there is a need to define new markers for bladder cancer. CLIC1 has not been previously studied in bladder cancer and thus, we aimed to assess its immunohistochemical expression in relation to different stages of bladder cancer development. MATERIALS AND METHODS: Immunohistochemistry for CLIC1 was applied in 50 cases of muscle invasive bladder cancer. RESULTS: CLIC1 was not expressed in the normal urothelium, but a strong reaction was observed in dysplastic urothelium, carcinoma in situ and in 94% of the cases with invasive urothelial carcinoma; however, it was not expressed in squamous cell carcinoma cases. No correlation was found between the immunohistochemical expression of CLIC1 and the stage and grade of the tumour. CONCLUSION: CLIC1 was overexpressed in urinary bladder dysplastic epithelium, carcinoma in situ and invasive carcinoma. CLIC1 constitutes a new potential marker of invasive bladder cancer.