INTRODUCTION: Micropapillary carcinoma (MPC) of the bladder is a rare and aggressive histologic variant of urothelial carcinoma (UC). At the time of presentation, most MPC are muscle invasive with frequent vascular invasion (VI). Our series explores protein expression of markers known to be indicators of poor clinical outcome and progression, trying to explain aggressiveness of MPC. PATIENTS AND METHODS: 18 patients with MPC were reviewed. We explored protein expression of p53, MIB-1, Aurora-A and survivin in MPC and compared their expression to conventional urothelial carcinoma (CUC) of the same grade and stage. RESULTS: Patients, aged 46-85 years, underwent transurethral resection or cystoprostatectomy for UC. MPC was either pure (39%) or only partially present (61%). 55% of the patients died. VI was seen in 95%. MPC displayed overexpression of p53 and MIB-1, Aurora-A and survivin. No statistically significant difference could be made with CUC except for Aurora-A (p = 0.03). CONCLUSIONS: This is the first study to explore different markers of bad clinical outcome in MPC. We suggest that Aurora-A via mechanisms implied into early steps of mitosis might play a role in aggressive clinical behavior of MPC. Copyright 2009 S. Karger AG, Basel.
INTRODUCTION:Micropapillary carcinoma (MPC) of the bladder is a rare and aggressive histologic variant of urothelial carcinoma (UC). At the time of presentation, most MPC are muscle invasive with frequent vascular invasion (VI). Our series explores protein expression of markers known to be indicators of poor clinical outcome and progression, trying to explain aggressiveness of MPC. PATIENTS AND METHODS: 18 patients with MPC were reviewed. We explored protein expression of p53, MIB-1, Aurora-A and survivin in MPC and compared their expression to conventional urothelial carcinoma (CUC) of the same grade and stage. RESULTS:Patients, aged 46-85 years, underwent transurethral resection or cystoprostatectomy for UC. MPC was either pure (39%) or only partially present (61%). 55% of the patients died. VI was seen in 95%. MPC displayed overexpression of p53 and MIB-1, Aurora-A and survivin. No statistically significant difference could be made with CUC except for Aurora-A (p = 0.03). CONCLUSIONS: This is the first study to explore different markers of bad clinical outcome in MPC. We suggest that Aurora-A via mechanisms implied into early steps of mitosis might play a role in aggressive clinical behavior of MPC. Copyright 2009 S. Karger AG, Basel.