Tight junctions and bladder cancer (review).

Tight junctions play a critical role in the maintenance of the urine-blood barrier creating a physiological barrier to the passage of ions and solutes between the urine and blood. Alterations in this urine-blood barrier function have been demonstrated in some diseases and regulation of the tight junction function has been recognised as an important aspect of the cell biology of cancer in terms of disease progression and as a potential therapeutic target. Although tight junctions play an important role in the physiological control of bladder function, there is little published on their molecular composition or regulation in the normal or diseased bladder. The purpose of this review is to summarise current understanding on the role and regulation of tight junction function in the normal and diseased bladder.

A case of laparoscopic ureteric reimplantation in a solitary urinary system.

Ureteric strictures can be caused by traumatic pelvic surgery, urolithiasis and instrumentation. There are various treatment options for ureteric stricture, including laparoscopic ureteric reimplantation. A 56-year-old female with a history of chronic left pelviureteric junction obstruction presented with urosepsis secondary to right-sided urolithiasis. The patient had a left nephrectomy and developed right-sided ureteric stricture following repeated ureteroscopy to manage her stone disease. The treatment with ureteric stenting was unsuccessful. Here we present a case on the feasibility of laparoscopic reimplantation for ureteric stricture in a solitary kidney to preserve renal function and avoid further ureteroscopy or nephrostomies.

Transurethral resection biopsy as part of a saturation biopsy protocol: a cohort study and review of the literature.

OBJECTIVE: To evaluate the prostate cancer (CaP) detection rate and morbidity of performing a transurethral resection biopsy of the prostate (TURBP) at the same time as a saturation biopsy (SBx). PATIENTS: A total of 102 men with previous negative transrectal ultrasound (TRUS) biopsies underwent a SBx under formal anaesthesia. Fifty-four [54 (52.9%)] had a combined SBx and TURBP (Group 1) and 48 (47.1%) had a SBx only (Group 2). RESULTS: The CaP detection rate in Group 1 was 38.9% (21/54), which was significantly higher than the detection rate of 27.1% (13/48) in Group 2 (P = 0.005). CaP was detected via TURBP in 12 patients (22.2%) from Group 1, including 8 (14.8%) patients who had CaP solely in their TURBP chips. According to the D'Amico classification, 66.6% (14/21) of the cancers in Group 1 were intermediate (n = 4) or high risk (n = 10). Of the 8 'TURBP only' cancers, 75% (6/8) were intermediate (n = 2) or high risk (n = 4). Seven of these eight patients went on to have a radical prostatectomy (RP) but only 2 (28.6%) were found to have a pure anterior/transition zone (TZ) tumor. The postoperative urinary retention and emergency admission rates for Groups 1 and 2 were 29.6% (16/54) vs. 16.6% (8/48) (P = 0.095) and 11.1% (6/54) vs. 5.5% (2/48) (n = 0.17). There was no difference in terms of hematuria (P = 0.54), urinary tract infection (UTI) (P = 0.22), or sepsis (P = 0.21), and patients in Group 1 spent an average of 0.5 days longer in hospital (1.9 vs. 1.4; P = 0.008). CONCLUSIONS: TURBP in association with SBx increases the detection of clinically important CaP. However, this does have to be balanced against the small increased incidence of urinary retention, emergency re-admission, and longer hospital stay.

Claudin-11 decreases the invasiveness of bladder cancer cells.

The expression of claudin-11 in benign and malignant bladder tissue and the effect of forced expression of claudin-11 on tight junction function and invasiveness of bladder cancer cells were studied. Claudin-11 expression was tested in bladder cancer cell lines (T24/83, RT 112/84 and EJ138) using reverse transcription-polymerase chain reaction (RT-PCR) and in benign and malignant bladder tissue by quantitative RT-PCR and immunohistochemistry. T24/83 cells were transfected with the pcDNA.1/NT-GFP-TOPO vector containing full-length human claudin-11 sequence. Stable-transfected cells overexpressing claudin-11 (T24Cl-11Ex), wild-type cells (T24WT) and the empty plasmid control clone (T24GFP) were compared using transurothelial resistance (TUR), in vitro adhesion, invasion and growth assays. Claudin-11 was strongly expressed in the non-invasive RT112/84 cell line compared to the invasive T24/83 and EJ138 TCC cell lines. Benign bladder tissue demonstrated equal expression of claudin-11 mRNA as carcinoma, but displayed more intense staining than malignant tissue on immunohistochemistry. Forced-expression of claudin-11 in T24/83 cells was confirmed by PCR, immunoprecipitation and by immunofluorescence, which demonstrated increased perinuclear claudin-11 staining. Forced expression of claudin-11 did not affect TUR (p = 0.243), but significantly reduced invasion (p = 0.001) while increasing cell matrix adhesion (p = 0.001) and growth rates (p = 0.001). The greater expression of claudin-11 in benign vs. malignant tissue and non-invasive vs. invasive cell lines, and its effect in reducing bladder cancer cell invasiveness suggests that claudin-11 may have a role in preventing cancer progression and may serve as a therapeutic target in reducing metastasis.