Inactivation of tumor suppressor p53 and pRb in urothelium by SV40 T antigen resulted in urothelial carcinoma, resembling human high-grade carcinoma in situ.
Between January 1999 and December 2008, 275 patients who received six BCG intravesical instillations for NMIBC (transitional cell carcinoma) after transurethral resection were assessed for differences in outcomes according to the level of p53 overexpression.
The aim of the present study was to investigate the effects of these two antineoplastic drugs on the apoptotic index and cell cycle kinetics of urinary bladder transitional carcinoma cell lines with wild-type or mutant TP53 (RT4: wild type for TP53; 5637 and T24: mutated TP53).
No mutations of FGFR3 in normal urothelium in the vicinity of urothelial carcinoma of the bladder harbouring activating FGFR3 mutations in patients with bladder cancer.
Alterations in p53 represent a highly promising marker of disease recurrence and cancer specific mortality after radical cystectomy for urothelial carcinoma of the bladder.
To determine the prognostic value of p53 gene mutations and P53 overexpression for predicting the incidence of recurrence, progression and long-term survival of patients with transitional cell carcinoma (TCC) of the bladder.
In this article, we review the roles of p53 pathways in bladder carcinogenesis and findings from recent studies of ours and other groups, and we discuss the clinical significance of the abrogation of p53 pathways in the treatment of urothelial carcinoma.
To evaluate the expression profile of vascular endothelial growth factor (VEGF), kinase-insert-domain-containing receptor (KDR) and p53 in patients from Northeastern China with transitional cell carcinoma (TCC) of bladder.
To evaluate the expression profile of vascular endothelial growth factor (VEGF), kinase-insert-domain-containing receptor (KDR) and p53 in patients from Northeastern China with transitional cell carcinoma (TCC) of bladder.
To analyze the correlation between the genotypic and phenotypic patterns of p53 in patients with transitional cell carcinoma (TCC) of the urinary bladder.
We investigated expression patterns of CD44s and CD44v6 in transitional cell carcinoma (TCC) of the urinary bladder in relation to tumour grade, proliferative activity, and immunoreactivity for p53.
This prompted our investigation to explore the global Alu methylation and the promoter methylation of the novel putative tumor suppressor genes caveolin-1 and hDAB2IP, and of p53 in transitional cell carcinomas (TCC), squamous cell carcinomas and undifferentiated small cell carcinomas of the urinary bladder.
Recently, the same FGFR3 mutations known from skeletal dysplasia syndromes and urothelial carcinoma have been shown to cause benign human skin tumors such as seborrheic keratoses and epidermal nevi.
This prompted our investigation to explore the global Alu methylation and the promoter methylation of the novel putative tumor suppressor genes caveolin-1 and hDAB2IP, and of p53 in transitional cell carcinomas (TCC), squamous cell carcinomas and undifferentiated small cell carcinomas of the urinary bladder.
The results were compared to the mutation frequency of TP53 in urine sediments from patients diagnosed with transitional cell carcinoma (TCC) of the bladder and healthy controls.
To examine the significance of the methylation level of the p53 target and tumour suppressor genes apoptotic protease activating factor-1 (APAF-1) and death-associated protein kinase-1 (DAPK-1) in 80 microdissected tumour samples from transitional cell carcinoma (TCC) of the bladder and 80 tumour samples from clear-cell renal cell carcinoma (RCC) as well as from non-tumourous bladder and kidney tissue.
Clonality was tested in 86 tumours from 25 patients with recurrent and multifocal superficial bladder transitional cell carcinomas (TCCs) using the analysis of TP53 mutations and of LOH in the 17p13 and 9p21 regions.