This study sought to evaluate the efficacy and safety of photoselective vaporisation (PVP) vs. transurethral resection of the prostate (TURP) for patients with benign prostatic hyperplasia (BPH). Eligible studies were identified from electronic databases (Cochrane Library, PubMed and EMBASE). The database search, quality assessment and data extraction were performed independently by two reviewers. Efficacy (primary outcomes: maximum urinary flow rate (Q max ), international prostate symptom score (IPSS), postvoid residual urine (PVR) and quality of life (QoL); secondary outcomes: operative time, hospital time and catheter removal time) and safety (complications, such as transfusion and capsular perforation) were explored by using Review Manager 5.0. Six randomized controlled trials (RCTs) and five case-controlled studies of 1398 patients met the inclusion criteria. A meta-analysis of the extractable data showed that there were no differences in IPSS, Q max , QoL or PVR between PVP and TURP (mean difference (MD): prostate sizes ,70 ml, Q max at 24 months, MD50.01, P50.97; IPSS at 12 months, MD50.18, P50.64; QoL at 12 months, MD520.00, P50.96; PVR at 12 months, MD50.52, P50.43; prostate sizes .70 ml, Q max at 6 months, MD523.46, P50.33; IPSS at 6 months, MD53.11, P50.36; PVR at 6 months, MD525.50, P50.39). PVP was associated with a shorter hospital time and catheter removal time than TURP, whereas PVP resulted in a longer operative time than TURP. For prostate sizes ,70 ml, there were fewer transfusions, capsular perforations, incidences of TUR syndrome and clot retentions following PVP compared with TURP. These results indicate that PVP is as effective and safe as TURP for BPH at the mid-term patient follow-up, in particular for prostate sizes ,70 ml. Due to the different energy settings available for green-light laser sources and the higher efficiency and performance of higher-quality lasers, large-sample, long-term RCTs are required to verify whether different energy settings affect outcomes. INTRODUCTIONBenign prostatic hyperplasia (BPH) is a major cause of lower urinary tract symptoms (LUTSs) in men, especially in individuals over the age of 50 years. 1 LUTS secondary to BPH is typically characterized as voiding symptoms, such as weak stream, hesitancy, intermittency and incomplete emptying, storage symptoms, such as urgency, frequency and nocturia, and postmicturition symptoms. 2,3 Currently, the main treatment options for BPH include pharmacological therapy, such as a-adrenergic blockers and 5a-reductase inhibitors, or surgery, such as transurethral resection of the prostate (TURP), transurethral incision of the prostate and open simple prostatectomy. 4 Although TURP is the current 'gold standard' treatment for moderate-to-severe LUTS secondary to BPH, 5,6 the procedure has some limitations. Several studies 7,8 have demonstrated that the rate of complications following TURP, including transfusions, infections, urethral strictures, sexual dysfunction, urinary incontinence, urinary retention

Background The previous works about safety evaluation for constructed bladder tissue specific adenovirus are poorly documented. Thus, we investigated the biodistribution and body toxicity of bladder specific oncolytic adenovirus Ad-PSCAE-UPII-E1A (APU-E1A) and Ad-PSCAE-UPII-E1A-AR (APU-E1A-AR), providing meaningful information prior to embarking on human clinical trials. Materials and Method Conditionally replicate recombinant adenovirus (CRADs) APU-E1A, APU-EIA-AR were constructed with bladder tissue specific Uroplakin II (UP II) promoter to induce the expression of Ad5E1A gene and E1A-AR fusing gene, and PSCAE was inserted at upstream of promoter to enhance the function of promoter. Based on the cytopathic and anti-tumor effect of bladder cancer, these CRADs were intratumorally injected into subcutaneous xenografts tumor in nude mice. We then determined the toxicity through general health and behavioral assessment, hepatic and hematological toxicity evaluation, macroscopic and microscopic postmortem analyses. The spread of the transgene E1A of adenovirus was detected with RT-PCR and Western blot. Virus replication and distribution were examined with APU-LUC administration and Luciferase Assay. Results General assessment and body weight of the animals did not reveal any alteration in general behavior. The hematological alterations of groups which were injected with 5×108 pfu or higher dose (5×109 pfu) of APU-E1A and APU-E1A-AR showed no difference in comparison with PBS group, and only slight increased transaminases in contrast to PBS group at 5×109 pfu of APU-E1A and APU-E1A-AR were observed. E1A transgene did not disseminate to organs outside of xenograft tumor. Virus replication was not detected in other organs beside tumor according to Luciferase Assay. Conclusions Our study showed that recombinant adenovirus APU-E1A-AR and APU-E1A appear safe with 5×107 pfu and 5×108 pfu intratumorally injection in mice, without any discernable effects on general health and behavior.

The high frequency of recurrence and poor survival rate of bladder cancer demand exploration of novel strategies. Gene therapy via adenovirus has shown promising potential for the treatment of tumors. We constructed a bladder cancer-specific adenovirus carrying E1A-androgen receptor (AR) under the control of UPII promoter and prostate stem cell antigen enhancer (PSCAE), designated as Ad/PSCAE/UPII/E1A-AR, and investigated its antitumor effects in vitro and in vivo. We demonstrated that Ad/PSCAE/UPII/E1A-AR could be selectively replicated in bladder tumor cell lines (5637, BIU87, EJ and T24) when compared with control adenovirus Ad/PSCAE/UPII/Luc. However, there was no evidence of cytotoxicity for normal human bladder cell line SV-HUC-1 and hepatoma cell line SMMC7721. AR agonist R1881 could strengthen the oncolytic effect of Ad/PSCAE/UPII/E1A-AR in bladder cancer cells. In addition, we demonstrated that intratumoral injection of Ad/PSCAE/UPII/E1A-AR into established subcutaneous human EJ tumors in nude mice could significantly regress the growth of tumor and markedly prolong survival for tumor-bearing mice; on the other hand, saline-treated tumors continued to grow rapidly. Our studies indicate that Ad/PSCAE/UPII/E1A-AR could effectively treat bladder cancer in vitro and in vivo. Furthermore, our findings provide a promising therapeutic modality for the treatment of bladder cancer.

Heat shock protein 27 (HSP27), a regulator of cell survival, can enhance the resistance of cancer cells to radiotherapy. As microRNA-541-3p (miR-541-3p) was recently predicted to be a putative upstream modulator of HSP27, the present study was designed to investigate the function and mechanism underlying how miR-541-3p modulates the radiosensitivity of prostate cancer (PCa) cells by regulating HSP27. Through quantitative PCR, miR-541-3p was determined to be poorly expressed in PCa tissues relative to normal controls, whereas its expression was enhanced after radiotherapy. Consistently, miR-541-3p expression levels in PCa cells were elevated after radiation. Cell viability and proliferation and apoptosis under radiation were subsequently evaluated in response to loss-of-function of miR-541-3p. It was found that inhibition of miR-541-3p facilitated the viability and proliferation of PCa cells and promoted their apoptosis post radiation, hence reducing the radiosensitivity of LNCaP cells. Dual-luciferase reporter assay identified that miR-541-3p negatively regulated the HSP27 mRNA expression by targeting its 3′-UTR. Meanwhile, miR-541-3p overexpression inhibited the β-catenin expression by targeting HSP27. Furthermore, HSP27 or β-catenin overexpression was noted to significantly reverse the miR-541-3p-mediated changes in the biological functions of PCa cells post radiation, suggesting that HSP27-dependent activation of β-catenin might be the mechanism responsible for the promotive effect of miR-541-3p on radiosensitivity. Collectively, this study suggests that miR-541-3p specifically inhibits the HSP27 expression and downregulates β-catenin, thereby enhancing the radiosensitivity of PCa cells. Our findings highlight the underlying mechanism of the miR-541-3p/HSP27/Wnt/β-catenin axis regarding radiotherapy for PCa.

Our results proved synergistic antitumor effect of adenovirus Ad-PSCAE-UPII-E1A and radiation, which might be a potential therapeutic strategy for bladder cancer.