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Background: The six-transmembrane epithelial antigen of the prostate 3 (STEAP3) plays an essential role in iron uptake as an iron reductase. Previous studies found that STEAP3 may play crucial roles in tumorigenesis. However, a comprehensive pan‐cancer analysis of the prognosis and immunity of STEAP3 has not yet been reported. Methods: We performed a systematic analysis of the prognosis and immunity of STEAP3 in human pan-cancer. The data analysis and visualization were completed with R and Cytoscape. STEAP3 expression in cell lines and tissues was measured in multiple ways. Functional validation experiments were performed by shRNA knockdown inA498 and 786-O cell lines. Cell proliferation and invasive ability was detected by CCK-8 assay, transwell assay and wound healing assay. Results: In most tumor tissues, STEAP3 expression was remarkably upregulated and correlated with prognosis, particularly in clear cell renal cell carcinoma (ccRCC). Furthermore, STEAP3 expression was closely correlated with immune infiltrates and may induce recruitment and polarization of M2 macrophages in ccRCC. STEAP3 may be valuable for predicting responses to immune-checkpoint blockade (ICB) therapy. In addition, enrichment analysis results indicated that STEAP3 was positively related to immune-related pathways, P53 pathways and epithelial-mesenchymal transition (EMT). Finally, we demonstrated that STEAP3 was highly expressed in ccRCC tissues and might stimulate EMT via the downregulation of CDH1 in vitro in ccRCC. Conclusion: STEAP3 might function as a prognostic biomarker and immunotherapy response predictor in various cancers. Especially in ccRCC, STEAP3 is a new prognostic biomarker and exerts tumor-promoting function via stimulating the invasion and EMT and inducing recruitment and polarization of M2 macrophages.

With the increasing prevalence of obesity worldwide, obesity-related female stress urinary incontinence (FSUI) has become a key health problem. Recent studies indicated that FSUI is primarily caused by obesity-related pathological changes, such as fat droplet deposition, and results in pelvic floor nerve, vascular, and urethral striated muscle injury. Meanwhile, treatments for obesity-associated FSUI (OA-FSUI) have garnered much attention. Although existing OA-FSUI management strategies, including weight loss, pelvic floor muscle exercise, and urethral sling operation, could play a role in symptomatic relief; they cannot reverse the pathological changes in OA-FSUI. The continued exploration of safe and reliable treatments has led to regenerative therapy becoming a particularly promising area of researches. Specifically, micro-energy, such as low-intensity pulsed ultrasound (LIPUS), low-intensity extracorporeal shock wave therapy (Li-ESWT), and pulsed electromagnetic field (PEMF), have been shown to restore the underlying pathological changes of OA-FSUI, which might be related by regulation endogenous stem cells (ESCs) to restore urine control function ultimately in animal experiments. Therefore, ESCs may be a target for repairing pathological changes of OA-FSUI. The aim of this review was to summarize the OA-FSUI-related pathogenesis, current treatments, and to discuss potential therapeutic options. In particular, this review is focused on the effects and related mechanisms of micro-energy therapy for OA-FSUI to provide a reference for future basically and clinical researches.

To optimise the diagnosis and treatment of primary renal leiomyosarcoma, we present our experience with a similar case and review the literature. A 49-year woman was incidentally found to have a palpable mass in the right kidney. CT scan revealed an enhancing, heterogeneous, 6×7×9 cm right renal mass. On suspicion of renal carcinoma, a right radical nephrectomy was performed. The pathological diagnosis was primary renal leiomyosarcoma. After 40 months of regular follow-up, local recurrence was found, and she had liver metastases. She died of cachexia due to tumor metastasis, and the survival period was just 44 months. With unobvious clinical manifestations, preoperative imaging and postoperative pathological examination might be helpful for an accurate diagnosis. Radical nephrectomy to completely remove the tumor is recommended, and the combination of neoadjuvant or postoperative therapy should also be considered. Key Words: Renal neoplasms, Leiomyosarcoma, Diagnosis, Therapy.

Next generation antiandrogens such as enzalutamide (Enz) are effective initially for the treatment of castration-resistant prostate cancer (CRPC). However, the disease often relapses and the underlying mechanisms remain elusive. By performing H3-lysine-27 acetylation (H3K27ac) ChIP-seq in Enz-resistant CRPC cells, we identified a group of super enhancers (SEs) that are abnormally activated in Enz-resistant CRPC cells and associated with enhanced transcription of a subset of tumor promoting genes such as CHPT1, which catalyzes phosphatidylcholine (PtdCho) synthesis and regulates choline metabolism. Increased CHPT1 conferred CRPC resistance to Enz in vitro and in mice. While androgen receptor (AR) primarily binds to a putative CHPT1 enhancer and mediates androgen-dependent expression of CHPT1 gene in Enz-sensitive prostate cancer cells, AR binds to a different enhancer within the CHPT1 SE locus and facilities androgen-independent expression of CHPT1 in Enz-resistant cells. We further identified a long-non coding RNA transcribed at CHPT1 enhancer (also known as enhancer RNA) that binds to the H3K27ac reader BRD4 and participates in regulating CHPT1 SE activity and CHPT1 gene expression. Our findings demonstrate that aberrantly activated SE upregulates CHPT1 expression and confers Enz resistance in CRPC, suggesting that SE-mediated expression of downstream effectors such as CHPT1 can be viable targets to overcome Enz resistance in PCa.

Background Previous study has reported that loss of epithelial androgen receptor (AR) may promote tumor progression and cause TRAMP mouse model die earlier. The detail mechanisms, however, remain unclear. Methods Immunohistochemistry assay, Western blot and real-time PCR were used to detect the expression of epithelial and mesenchymal markers. RNA extraction, RT-PCR, quantitative RT-PCR, BrdU incorporation assays, flow cytometry and other experimental technics were also used in present work. Results Decreased expression of epithelial markers (Cytokeratin 8, NKX3.1 and E-cadherin) and increased expression of mesenchymal markers (α-SMA, Vimentin, and N-cadherin) in were found in AR knockout TRAMP tumors. Further investigation indicated that AR signal deprivation is associated with cell morphology transition, high cell mobility, high cell invasion rate and resistance to anoikis in TRAMP prostate tumor cells. Together, these findings implied knockout AR in TRAMP prostate tumor may lead to EMT, which may result in earlier metastasis, and then cause TRAMP mice die earlier. TGF-β1 is responsible for EMT in AR knockout TRAMP tumor cells. Conclusions In conclusion, ADT therapy induced hormone refractory prostate cancer may gain the ability of metastasis through cell's EMT which is a phase of poor differentiation. Anti-EMT drugs should be developed to battle the tumor metastasis induced by ADT therapy.

Purpose This study sought to identify factors associated with survival of pT1 urothelial carcinoma of bladder (UCB) after radical cystectomy (RC). Methods This study consists of 114 pT1 UCB [primary 83, recurrent 31, none were amenable to transurethral resection (TUR)] treated by radical cystectomy. Survival analysis using Cox regression tests were performed to identify factors associated with survival of pT1 UCB after RC. Results Pelvic lymph node (LN) status, age and lymphovascular invasion (LVI) are associated with survival of pT1 UCB after RC; recurrent pT1 UCB of high grade origin (HGO) tends to have poorer CSS than primary pT1 UCB or recurrent pT1 UCB of low grade origin (LGO) (5-year and 10-year CSS rates was 75% and 73% for primary cases; 77% and 77% for recurrent pT1 UCB of LGO; and 56% and 37% for recurrent pT1 UCB of HGO, p = 0.078). Conclusions LN status, age and LVI were significantly associated with survival of pT1 UCB after RC. Recurrent pT1 UCB of HGO should be managed with radical cystectomy in a timely fashion given that these cases tend to have poorer CSS than primary pT1 UCB after RC, even if they did not progress to muscle-invasive bladder cancer (MIBC).

Purpose In recent years, there has been an increase in the incidence of small renal masses (SRMs) and nephrectomy was the standard management of this disease in the past. Currently, the use of active surveillance has been recommended as an alternative option in the case of some patients with SRMs due to its heterogenicity. However, limited studies focused on the regarding risk stratification. Therefore, in the current study, we developed a nomogram for the purpose of predicting the presence of high-grade SRMs on the basis of the patient information provided (clinical information, hematological indicators, and CT imaging data). Patients and methods A total of 329 patients (consisting of development and validation cohort) who had undergone nephrectomy for SRMs between January 2013 and May 2016 retrospectively were recruited for the present study. All preoperative information, including clinical predictors, hematological indicators, and CT predictors, were obtained. Lasso regression model was used for data dimension reduction and feature selection. Multivariable logistic regression analysis was applied for the establishment of the predicting model. The performance of the nomogram was assessed with respect to its calibration and discrimination properties and externally validated. Results The predictors used in the assessment of the nomogram included tumor size, CT tumor contour, CT necrosis, CT tumor exophytic properties, and CT collecting system oppression. Based on these parameters, the nomogram was evaluated to have an effective discrimination and calibration ability, and the C-index was found to be 0.883 after internal validation and 0.887 following external validation. Conclusion Based on the aforementioned findings, it can be concluded that CT imaging-based preoperative nomogram is an effective predictor of SRMs and hence can be used in the preoperative evaluation of SRMs, due to its calibration and discrimination abilities.

To systematically analyze histopathologic features of pseudocapsule in small renal cell tumor (diameter≤4cm), assess the integrity of pseudocapsules by Computed Tomography (CT), and provide theoretical basis for the safety of nephron sparing surgery.The pathological data of 116 patients who underwent surgery with clear cell renal cell carcinoma admitted from May 2010 to October 2017 were retrospectively analyzed. All patients underwent a CT scan of the abdomen including an unenhanced and triple-phase (arterial, nephrographic and excretory) post contrast series."All patients underwent a CT scan of the abdomen including an unenhanced and triple-phase (arterial, nephrographic and excretory) post contrast series."All patients underwent a CT scan of the abdomen including an unenhanced and triple-phase (arterial, nephrographic and excretory) post contrast seriesAll patients underwent a CT scan of the abdomen including an unenhanced and three-phase (arterial, nephrographic and excretory) post contrast series. Thorough gross examination and histological sections were used to determine the integrity of the pseudocapsule by two uropathologists. The consistency between pathological findings and CT imaging were evaluated by Kappa consistency test.The mean diameter of tumor was 3.0cm, range (2.6 ± 0.8) cm. On CT the pseudocapsule can present with one of the three following feathers:1) A regular and distinct halo; 2)lobulated clear margins;3) blurred margins. On histopathology, complete psuedocapsule was found in 85 tumors, incomplete psuedocapsule in 25 and no psuedocapsule was found in 6 tumors; CT scan findings demonstrated a regular halo in 82 tumors, lobulated clear margins in 26 and blurred margins in 8 tumors(Kappa=0.833,P=0.000).Most small renal cell tumors have an obvious psuedocapsule. Preoperative determination of the psuedocapsule's integrity is particularly important. CT scan can reliably evaluate the tumor margins and demonstrate the psuedocapsule when present. The imaging results are well correlated with the pathologic findings.

With the continuous integration and intersection of life sciences, engineering and physics, the application for micro-energy in the basic and clinical research of regenerative medicine (RM) has made great progress. As a key target in the field of RM, stem cells have been widely used in the studies of regeneration. Recent studies have shown that micro-energy can regulate the biological behavior of stem cells to repair and regenerate injured organs and tissues by mechanical stimulation with appropriate intensity. Integrins-mediated related signaling pathways may play important roles in transducing mechanical force about micro-energy. However, the complete mechanism of mechanical force transduction needs further research. The purpose of this article is to review the biological effect and mechanism of micro-energy treatment on stem cells, to provide reference for further research.

Purpose In recent years, there has been an increase in the incidence of small renal masses (SRMs) and nephrectomy was the standard management of this disease in the past. Currently, the use of active surveillance has been recommended as an alternative option in the case of some patients with SRMs due to its heterogenicity. However, limited studies focused on the regarding risk stratification. Therefore, in the current study, we developed a nomogram for the purpose of predicting the presence of high-grade SRMs on the basis of the patient information provided (clinical information, hematological indicators, and CT imaging data). Patients and methods A total of 329 patients (consisting of development and validation cohort) who had undergone nephrectomy for SRMs between January 2013 and May 2016 retrospectively were recruited for the present study. All preoperative information, including clinical predictors, hematological indicators, and CT predictors, were obtained. Lasso regression model was used for data dimension reduction and feature selection. Multivariable logistic regression analysis was applied for the establishment of the predicting model. The performance of the nomogram was assessed with respect to its calibration and discrimination properties and externally validated. Results The predictors used in the assessment of the nomogram included tumor size, CT tumor contour, CT necrosis, CT tumor exophytic properties, and CT collecting system oppression. Based on these parameters, the nomogram was evaluated to have an effective discrimination and calibration ability, and the C-index was found to be 0.883 after internal validation and 0.887 following external validation. Conclusion Based on the aforementioned findings, it can be concluded that CT imaging–based preoperative nomogram is an effective predictor of SRMs and hence can be used in the preoperative evaluation of SRMs, due to its calibration and discrimination abilities.

Background: As deregulation of androgen receptor (AR) signaling target genes is associated with tumorigenesis and the development of prostate cancer (PCa), AR signaling is the primary therapeutic target for PCa. Although patients initially responses to first-line androgen deprivation therapies (ADTs), most of them with advanced PCa progress to lethal castration-resistant prostate cancer (CRPC). Recent studies have suggested the molecular mechanisms by which AR elicit the robust up-regulation of the FKBP51 gene. We suggest that restored expression of FKBP51 gene, modulated by androgen receptor splicing variant 7 (AR- V7) which replaces full length androgen receptor (AR-FL) in androgen ablation status, promotes CRPC progression through activating NF-κB signaling. Methods: Immunohistochemistry assays were used to detect the expression of AR-V7, FKBP51 and NF-κB signaling correlated proteins in CRPC tissues. An androgen ablation resistant PCa cell line model established by Long-term culturing in androgen depleted medium, named androgen-independent LNCaP (LNCaP-AI) cells, were used to dynamically monitor FKBP51 expression during the process of androgen dependent PCa cells transforming into androgen-independent cells, as well as its association with NF-κB signal pathway. LNCaP-AI cell line was determined to express AR-V7 protein continuously. Luciferase reporter assays and DNA pull down were used to determine the association between AR-V7 and FKBP51. Results: Our results suggested that CRPC patients with AR-V7 high expression tend to have higher expression of FKBP51 and enhanced NF-κB signaling compared with AR-V7 negative patients. Knockdown of AR-V7 or FKBP51 in LNCaP-AI cells attenuated the level of p-NF-κB (Ser536) and androgen- resistant cells growth. Luciferase reporter assays and DNA pull down results indicated that FKBP51 was transcriptionally promoted by AR-V7 in absence of androgen, which enhanced NF-κB signaling. Conclusions: Because of upregulation of AR-V7 in androgen-independent PCa cells, increasing of FKBP51 induced NF-κB signaling, leading to progression of CRPC.

Renal cell carcinoma (RCC) is a common urologic tumor and the third leading cause of death among urological tumors. Recent studies demonstrate that RCC tumors are more heavily infiltrated by lymphocytes than other cancers. However, the exact roles played by CD4 + T cells in RCC proliferation remain unknown. In this study, we cocultured RCC cells with CD4 + T cells. Stable knockdown of YBX1 in RCC cells was constructed. The effects of CD4 + T cells, TGFβ1 and YBX1 on RCC cells were investigated using cell viability assays. In situ RCC nude mouse model was used to observe the tumor growth. The potential mechanisms of CD4 + T cells and YBX1 in RCC cells proliferation were explored by qRT-PCR and western blot. Expression of CD4, Foxp3 and TGFβ1 in RCC were quantified by immunohistochemical staining. The results indicated that CD4, Foxp3 and TGFβ1 were significantly up-regulated in RCC tissues. Human clinical sample and in vitro cell lines studies showed that RCC cells had better capacity than its surrounding normal kidney epithelial cells to recruit the CD4 + T cells. In vivo mouse model studies were consistent with the results by in vitro cell lines studies showing infiltrating T cells enhanced RCC cell proliferation. qRT-PCR and western blot exhibited that CD4 + T cells could enhance RCC cell proliferation via activating YBX1/HIF2α signaling pathway. Furthermore, CD4 + T cells functioned through inducing TGFβ1 expression. In a word, infiltrating CD4 + T cells promoted TGFβ1 expression in both RCC and T cells and regulated RCC cells proliferation via modulating TGFβ1/YBX1/ HIF2α signals.

Transforming growth factor-β1 (TGFβ1) plays a significant role in regulating cellular proliferation and apoptosis. A large number of studies related to the association between TGFβ1 Leu10Pro polymorphism and prostate cancer (PC) risk, but get conflicting results. We performed a meta-analysis based on six studies, assessing the strength of the association using odds ratios (OR) with 95 % confidence intervals (CI). Overall, our evidence has indicated that TGFβ1 Leu10Pro polymorphism had significantly increased PC risk in the allele comparison model (OR = 1.081, 95 % CI = 1.003–1.165, P heterogeneity = 0.141, P = 0.041). In the stratified analysis by ethnicity, the same results were found among Caucasians (for heterozygote model, OR = 1.741, 95 % CI = 1.004–3.020, P heterogeneity = 0.000, P = 0.049; recessive model, OR = 1.339, 95 % CI = 1.045–1.717, P heterogeneity = 0.020, P = 0.021; allele comparison model, OR = 1.091, 95 % CI = 1.005–1.184, P heterogeneity = 0.048, P = 0.037). In conclusion, this meta-analysis suggested that TGFβ1 Leu10Pro polymorphism contributed to the development of PC. A well-designed and larger study is still required to evaluate this polymorphism and PC risk.

Homeobox (Hox) genes encode homeodomain-containing transcription factors critical to development, differentiation, and homeostasis. Their dysregulation has been implicated in various cancers. In the present study, we show that HoxB3 mRNA and protein are overexpressed in primary prostate cancer tissues compared to the adjacent normal prostate tissues. Moreover, HoxB3 overexpression is associated with higher Gleason grade (⩾7) (P=0.002), clinical stage (P

Objective Transumbilical single incision surgery (TSIS) has recently gained popularity for symptomatic renal cysts. We evaluated the clinical utility and safety of homemade glove port device in bilateral renal cyst decortication patients at our institution. Methods We reviewed our series of 42 bilateral symptomatic renal cyst (range, 4–12 cm) decortication performed from November 2010 to December 2013. A homemade port device consisted of two control loops and a glove to form three channels was placed through the umbilical single incision. A homemade single port device was made by fixing a size 7 1/2 surgical glove to the retractor outer ring and securing the glove fingers to the end of three trocars with a tie. The homemade port was inserted at the umbilical incision, operation was performed by using a special flexible 30-degree laparoscope and conventional laparoscopic instruments. Results All cases were completed successfully, without conversion to a standard laparoscopic or open approach. The average operative time was 75 min and the estimated blood loss was less than 30 mL, no intraoperative complication occurred. The mean hospital stay was 2.8 d lap[2–5] days, with a median follow-up of 20 months (range, 8–32) there was no recurrence. Conclusions Our homemade single port device is cost-effective and more flexible to deal with bilateral renal cysts especially ventral lesions than the current multichannel port or traditional laparoscopic surgery.

PRDXs are antioxidant enzymes that have an important role in cell differentiation, proliferation and apoptosis. We investigated whether PRDX I and VI expression is related to bladder cancer.PRDX I and VI mRNA levels were examined in 149 tumor specimens in patients with primary bladder cancer, in 19 specimens with corresponding normal-appearing bladder mucosa surrounding cancer and in 18 with normal bladder mucosa using real-time polymerase chain reaction.PRDX I and VI expression in bladder cancer (0.6644 and 0.1455 pg/ml) was significantly higher than in normal tissue (0.0278 and 0.0542 pg/ml, each p0.05) and higher than in corresponding normal bladder mucosa surrounding cancer (0.2353 and 0.0304 pg/ml, respectively, each p0.0005). PRDX I and VI expression was enhanced in patients with no recurrence (0.8148 and 0.2232 pg/ml) and no progression (0.7405 and 0.1716 pg/ml) compared with levels in those with recurrence (0.4314 and 0.0588 pg/ml) and progression (0.4338 and 0.0668 pg/ml, respectively, each p0.05). PRDX I and VI expression did not correlate with disease-free survival in patients with bladder cancer.Enhanced PRDX I and VI expression is strongly associated with bladder cancer development. Moreover, enhanced PRDX I and VI expression is also positively associated with a low rate of bladder cancer recurrence and progression. It might be useful as a marker for assessing the recurrence or progression of human bladder cancer.

RUNX3 is inactivated at high frequency in many tumors. However, in most cases, inactivation is caused by silencing of the gene due to promoter hypermethylation. Because epigenetic silencing is known to affect many major tumor suppressor genes in cancer cells, it is not clear whether RUNX3 is primarily responsible for the induction of carcinogenesis in these cases, except for the gastric cancer cases that we reported previously. We investigated genetic and epigenetic alterations of RUNX3 in 124 bladder tumor cases and seven bladder tumor–derived cell lines. Here we show that RUNX3 is inactivated by aberrant DNA methylation in 73% (90 of 124) of primary bladder tumor specimens and 86% (six of seven) of bladder tumor cell lines. In contrast, the promoter regions of 20 normal bladder mucosae were unmethylated. Importantly, one patient bore missense mutations, each of which resulted in amino acid substitutions in the highly conserved Runt domain. The mutations abolished the DNA-binding ability of RUNX3. A second patient had a single nucleotide deletion within the Runt domain coding region that resulted in truncation of the protein. RUNX3 methylation was a significant risk factor for bladder tumor development, superficial bladder tumor recurrence, and subsequent tumor progression. These results strongly suggest that inactivation of RUNX3 may contribute to bladder tumor development and that promoter methylation and silencing of RUNX3 could be useful prognostic markers for both bladder tumor recurrence and progression.

Transitional cell carcinoma of the urinary bladder has a diverse collection of biologic and functional characteristics. This is reflected in differing clinical courses. The diagnosis of bladder cancer is based on the information provided by cystoscopy, the gold standard in combination with urinary cytology findings. Many tumor markers have been evaluated for detecting and monitoring the disease in serum, bladder washes, and urinary specimens. However, none of these biomarkers reported to date has shown sufficient sensitivity and specificity for the detection of the whole spectrum of bladder cancer diseases in routine clinical practice. The limited value of established prognostic markers requires the analysis of new molecular parameters of interest in predicting the prognosis of bladder cancer patients; in particular, the high-risk patient groups at risk of progression and recurrence. Over the past decade, there has been major progress elucidating of the molecular genetic and epigenetic changes leading to the development of transitional cell carcinoma. This review focuses on the recent advances of genetic and epigenetic aspects in bladder cancer, and emphasizes how molecular biology would be likely to affect the future therapies.

Objectives Laparoscopic nephropexy has been reported as a minimally invasive approach for symptomatic nephroptosis. We performed five cases of laparoscopic nephropexy using a self-made polytetrafluoroethylene “basket” to fix the inferior parts of kidneys to 12th rib. Methods All patients (four women and one man) had symptomatic nephroptosis presenting with flank pain, repeat hemoturine or hydronephrosis. Preoperative ultrasonography, intravenous urography and renal CT scan in supine and upright positions were done for nephroptosis diagnosis. Transperitoneal laparoscopic nephropexy were carried out using self-prepared “basket” made of stripes cutting from polytetrafluoroethylene herniorrhaphy mesh. After the kidney was completely dissected from surrounding perirenal fat, it was put into the non-absorbable polytetrafluoroethylene “basket” through multiple suturing and fixation to renal capsule. Then suspended the kidney by fixation the lower pole of kidney to the twelfth rib, and reinforced by suturing the posterior surface of the kidney to the quadratus lumborum muscle. Results The operation was successfully completed laparoscopically in all cases without major perioperative complications. The average operative time was 95 minutes, and the mean estimated blood loss was less than 60 mL. Hospital stay was 4.5 days (range, 3–6 days). Postoperative urography or ultrasound revealed complete resolution of loin pain and nephroptosis with a median follow-up of 8 months (range, 2–15 months). Conclusions Laparoscopic nephropexy using self-made polytetrafluoroethylene “basket” with a modified three-point fixation technique is an effective minimally invasive procedure for treating symptomatic nephroptosis with excellent short-term results.

Laparoscopic Madigan prostatectomy have not been reported yet. We modified the Madigan prostatectomy to make it suitable for laparoscopically enucleating hyperplastic glands larger than 100 g.Between May 2007 and Oct 2008, extraperitoneal laparoscopic prostatectomy with maintenance of the intact urethra had been performed on 16 patients with benign prostatic hyperplasia (BPH) and glands larger than 100 mg. To make it suitable for laparoscopic use, two major modifications had been made: (1) Open the prostate capsule near the bladder neck without sutures along the opening; (2) identify the bladder neck mucosa before recognizing the urethra. All patients were evaluated preoperatively and postoperatively. Data were compared with those from open surgeries.All laparoscopic procedures were successful with the total operative time of 111.8±28.6 minutes, which had no significant difference compared with open surgeries. Estimated blood loss of laparoscopic procedures (112.5±47.8 mL) was significantly lower than that of open surgery. The catheterization time and hospital stay time was significantly shorter than open surgery. The improvement of the International Prostate Symptom Score, maximum flow rate, and quality-of-life score were not different between the comparing groups.The laparoscopic Madigan prostatectomy is a safe and feasible approach for large glands (BPH). Furthermore, its advantages include shorter learning curve, reduced blood loss, less retroejaculation rate, shorter catheterization time, and shorter hospital stay.

Acetylation of chromatin interacting proteins is central to the epigenetic regulation of gene expression. Various tumor suppressors are inactivated by abnormal epigenetic modification. A great deal of effort has been devoted to developing anticancer agents that reactivate silenced tumor suppressors by modulating chromatin structure. Studies show that histone deacetylase inhibitors can act as anticancer agents and several histone deacetylase inhibitors are currently in clinical trials. We noted that the tumor suppressor RUNX3 is inactivated by promoter hypermethylation in human bladder cancer. We investigated whether reactivation of RUNX3 could suppress bladder cancer development in an animal model.We analyzed RUNX3 reactivation and protein stabilization by a mild inhibitor of class III histone deacetylases, nicotinamide, by immunoprecipitation and immunoblot. Mouse bladder tumor was induced by N-butyl-N-(4-hydroxybutyl) nitrosamine. The effect of nicotinamide on Runx3 methylation status and tumor growth was measured.Nicotinamide induced RUNX3 expression at the transcriptional and posttranslational levels in a carcinogen induced mouse bladder tumor model and in human bladder tumor xenografts. Nicotinamide effectively inhibited the growth and progression of bladder tumors without decreasing body weight.Results suggest that nicotinamide has preventive and therapeutic effects on tumorigenesis through multiple mechanisms of RUNX3 expression up-regulation.

Objectives To determine whether polymorphisms of tumor necrosis factor-alpha ( TNF-α ), vascular endothelial growth factor ( VEGF ), human 8-oxoguanine DNA glycosylase 1 ( hOGG1 ), glutathione S-transferase-μ ( GSTM1 ), and glutathione S-transferase-φ ( GSTT1 ) are risk factors for bladder cancer among Koreans. Methods We performed polymerase chain reaction-restriction fragment length polymorphism and multiplex polymerase chain reaction in blood genomic DNA of 153 patients with primary bladder cancer and 153 control subjects. Results GSTM1 -negative, GSTT1 -positive, and hOGG1 Ser326Ser and Ser326Cys genotypes are risk factors for bladder cancer ( P = 0.020, P = 0.044, and P = 0.012, respectively). The cancer stage was significantly associated with the TNF-α genotype (GG versus GA and AA; P = 0.036). A notable correlation was observed between the VEGF genotype and grade ( P = 0.015). In patients with superficial bladder cancer, the hOGG1 genotype was related to recurrence. The hOGG1 Ser326Ser and Ser326Cys genotypes were risk factors for superficial bladder cancer recurrence compared with the Cys326Cys genotype ( P = 0.033, adjusted odds ratio 5.580, 95% confidence interval 1.145 to 27.183). Patients with the GSTM1 -positive genotype were at a 3.3-fold increased risk of cancer progression compared with those with the GSTM1 -negative genotype ( P = 0.009, adjusted odds ratio 0.303, 95% confidence interval 0.123 to 0.745). Conclusions Our data collectively suggest that these genetic polymorphisms may be useful as prognostic markers for bladder cancer in the clinical setting.

Purpose: We investigated whether the expression levels of Transforming growth factor β1 (TGF-β1) and its receptors were related to the development, recurrence, progression and disease-free survival in the patients with bladder cancer. Materials and Methods: The mRNA levels of TGF-β1 and its receptors were examined in 102 tumor specimens from patients with primary bladder cancer, 29 corresponding normal bladder mucosae specimens surrounding these tumors and 15 normal bladder mucosae specimens by performing quantitative competitive PCR (QC-PCR). The protein levels of TGF-β1 and its receptors were investigated by performing immunohistochemical staining on sections cut from 86 archival bladder tissue paraffin blocks. Results: QC-PCR analysis showed that expressions of TGF-β1, TGF-β receptor I (TGF-βRI) and receptor II (TGF-βRII) in the superficial and low-grade bladder cancers were significantly higher than those in both the corresponding normal bladder mucosae surrounding the cancer (p= 0.0069, 0.0022 and 0.0046, respectively) and the control's normal bladder mucosae (p=0.0014, 0.0125 and 0.0089, respectively). Expressions of TGF-β1 and its receptors were enhanced in the non-recurred and non-progressed patients compared to the recurred cases (p=0.0022, 0.0003 and 0.0001, respectively) and the progressed cases (p=0.0002