TP53 gene mutations in prostate cancer progression.

Background: We assessed the predictive value of TP53 mutations and prostate-specific antigen (PSA) for tumor progression in prostate cancer (PCa) patients.

Materials And Methods: Ninety tumor tissue samples of patients with PCa from radical prostatectomy were used. Tumor progression was estimated biochemically by the PSA level (> 0.

TP53 gene mutations as an independent marker for urinary bladder cancer progression.

This study evaluates the influence of the TP53 genetic status on tumour recurrence and progression with a highly effective electrophoretic technique. DNA from tissue of 75 non-invasive urinary bladder cancers was PCR amplified in the TP53 exons 5-8 and run on horizontal polyacrylamide gels under defined temperature conditions to yield specific gel shifts. Kaplan-Meier and Cox-Regression analysis were performed with tumour progression.

Valproic acid, a histone deacetylase inhibitor, is an antagonist for oncolytic adenoviral gene therapy.

Oncolytic adenoviruses preferentially replicate in and lyse tumor cells. However, their application to cancer gene therapy has been complicated by the low levels of coxsackie and adenovirus receptor (CAR) expressed in many solid tumors. Histone deacetylase inhibitors (HDACIs) significantly up-regulate CAR expression in tumor cells and have additional antineoplastic activities.

Valproic acid inhibits invasiveness in bladder cancer but not in prostate cancer cells.

Histone deacetylase inhibitors (HDACIs) represent a promising new class of antineoplastic agents that affect proliferation, differentiation, and apoptosis in both solid and hematologic malignancies. In addition, HDACIs can alter the expression of at least one cellular adhesion molecule, the coxsackie and adenovirus receptor, in bladder cancer. Because HDACIs can increase expression of a known cellular adhesion molecule, we hypothesized that migration and/or invasion may also be affected.

Long-term benefit of 5-aminolevulinic acid fluorescence assisted transurethral resection of superficial bladder cancer: 5-year results of a prospective randomized study.

Purpose: As shown in various studies 5-aminolevulinic acid (ALA) induces fluorescence of malignant and dysplastic bladder tissue and increases tumor detection rates by about 20%. However, data on the long-term benefits are sparse. Thus, the 5-year outcome data of a prospective randomized trial comparing patients who initially underwent bladder tumor resection (TUR) under standard white light or with ALA induced fluorescence were evaluated.

Histone deacetylase inhibitors upregulate expression of the coxsackie adenovirus receptor (CAR) preferentially in bladder cancer cells.

Studies on bladder cancer cell lines have shown that low adenoviral (Ad) infectivity is associated with low-level coxsackie adenovirus receptor (CAR) expression. Recently, we and others demonstrated a tumor stage- and grade-dependent downregulation of CAR expression in a large series of clinical bladder cancer specimens. Here, we demonstrate adenoviral gene transfer can be markedly enhanced in bladder cancer cells by upregulation of CAR through the use of certain differentiating agents, including the histone deacetylase inhibitors (HDACI) trichostatin A and sodium phenylbutyrate.

Integrin alpha(v) and coxsackie adenovirus receptor expression in clinical bladder cancer.

Objectives: To evaluate the expression of the coxsackie and adenovirus receptor (CAR) and alpha(v) integrins in clinical specimens of bladder cancer to determine the susceptibility to adenoviral gene therapy. Efficient adenovirus-based gene therapy requires binding of the virus to CAR and involves the alpha(v) integrins. Studies on bladder cancer cell lines have shown that low adenoviral transduction rates were associated with low-level expression of CAR.