Objective To explore the clinical safety of maintaining oral anticoagulant therapy in patients with benign prostatic hyperplasia (BPH) undergoing thulium laser enucleation of the prostate (ThuLEP), and to provide evidence-based basis for perioperative anticoagulant management in clinical practice. Methods A retrospective analysis was performed on the clinical data of 186 BPH patients who underwent ThuLEP in the Department of Urology of our hospital from July 2023 to December 2024. According to the perioperative anticoagulant use protocol, the patients were divided into three groups: the anticoagulant maintenance group (62 cases, continued oral administration of original anticoagulants), the anticoagulant withdrawal group (61 cases, discontinued anticoagulants 7–10 days before surgery and received low-molecular-weight heparin bridging therapy), and the non-medication control group (63 cases, no history of long-term oral anticoagulant/antiplatelet therapy). Perioperative related indicators (operation time, intraoperative blood loss, hemoglobin decrease value), incidence of postoperative complications (bleeding, hematuria, urinary tract infection, thromboembolic events, etc.), as well as postoperative indwelling catheter time, length of hospital stay, and International Prostate Symptom Score (IPSS) and Quality of Life Score (QoL) at 1 month and 3 months after surgery were compared among the three groups. Results There were no statistically significant differences in preoperative general data (age, prostate volume, coagulation function, underlying diseases, etc.) among the three groups ( P > 0.05). There were no statistically significant differences in operation time [(68.5 ± 12.3) min vs (65.8 ± 11.7) min vs (66.2 ± 12.1) min], intraoperative blood loss [(52.3 ± 15.6) mL vs (49.7 ± 14.9) mL vs (48.9 ± 14.5) mL], and hemoglobin decrease value [(1.2 ± 0.4) g/dL vs (1.1 ± 0.3) g/dL vs (1.0 ± 0.3) g/dL] among the anticoagulant maintenance group, anticoagulant withdrawal group, and non-medication control group (all P > 0.05). There were no statistically significant differences in the incidence of postoperative bleeding, hematuria, urinary tract infection, or urinary incontinence among the three groups ( P > 0.05); no severe bleeding or blood transfusion cases occurred in any of the three groups. The incidence of postoperative thromboembolic events in the anticoagulant maintenance group (1.61%) was significantly lower than that in the anticoagulant withdrawal group (8.20%), with a statistically significant difference ( P < 0.05); no thromboembolic events occurred in the non-medication control group, which showed no statistically significant difference compared with the anticoagulant maintenance group ( P > 0.05) but a statistically significant difference compared with the anticoagulant withdrawal group ( P < 0.05). There were no statistically significant differences in postoperative indwelling catheter time or length of hospital stay among the three groups ( P > 0.05). At 1 month and 3 months after surgery, the IPSS score and QoL score of the three groups were significantly improved compared with those before surgery (P < 0.05), but there were no statistically significant differences among the groups ( P > 0.05). Conclusion Maintaining oral anticoagulant therapy in BPH patients undergoing ThuLEP does not increase the perioperative bleeding risk, but can significantly reduce the incidence of thromboembolic events. Its safety is equivalent to that of non-medication patients, and it does not affect the surgical efficacy or postoperative recovery, which is safe and feasible in clinical application.

At the transcriptomic level, several molecular subtyping schemes have been established to elucidate the intrinsic heterogeneity of urothelial carcinoma and to inform prognostic assessment and therapeutic guidance. However, a unified molecular classification scheme characterizing genomic alterations is lacking. Unsupervised and supervised clustering identified two distinct mutational signature subtypes. Kaplan-Meier analysis demonstrated that patients with the MUT2 subtype had a higher risk of death than those with the MUT1 subtype across multiple cohorts, including IMvigor210 (hazard ratio [HR], 1.74; 95% confidence interval [CI], 1.27-2.37; p < 0.001), UC-GENOME (HR, 1.54; 95% CI, 0.93-2.54; p = 0.091), The Cancer Genome Atlas (TCGA; HR, 1.45; 95% CI, 1.06-1.98; p = 0.020), MSK2022 (HR, 1.34; 95% CI, 1.10-1.64; p = 0.004), MSK2015 (HR, 3.43; 95% CI, 1.36-8.64; p = 0.005), and the Tongji cohort (HR, 4.99; 95% CI, 0.57-43.69; p = 0.11). Immunotherapy response rates were significantly higher in the MUT1 subtype than in the MUT2 subtype in IMvigor210 (31.8% vs. 13.1%; p = 0.003) and UC-GENOME (42.3% vs. 29.0%; p = 0.022). Consistent with these findings, single-cell analysis showed that MUT2 tumors were enriched in tumor-associated fibroblast subpopulations and had a lower abundance of immune effector cells. Overall, this genomic analysis identified two mutation-based subtypes of urothelial carcinoma associated with patient prognosis and immunotherapy response.

Clear cell renal cell carcinoma (ccRCC) is one of the most common malignancies. Recently, the role of brain-expressed X-linked 4 (BEX4) in cancer progression has received increasing attention. This study aimed to investigate the function of BEX4 in ccRCC and to reveal the underlying mechanisms. We first confirmed that BEX4 was significantly downregulated in ccRCC by bioinformatics analysis and that patients with low BEX4 expression tended to have prolonged overall survival time. Subsequently, we confirmed that BEX4 inhibited ccRCC cell proliferation in vitro and tumorigenesis in vivo through a series of cell function assays and the establishment of a nude mouse xenograft model, respectively. Mechanistically, we found that BEX4 positively regulates the expression of Src homology 2 domain-containing 4A (SH2D4A), an inhibitor of the NOTCH pathway, which further promoted the tumor-suppressive effects of BEX4. In addition, our study confirmed that the promoting effect of BEX4 on SH2D4A was achieved by inhibiting the deacetylase sirtuin 2 (SIRT2) activity. On this basis, we found that there was a competition between acetylation and ubiquitination modifications at the K69 site of SH2DA4 and that BEX4-induced upregulation of acetylation at the k69 site stabilizes SH2D4A protein expression by inhibiting ubiquitination at the same site. In addition, dual-luciferase assays showed that the transcriptional activity of BEX4 was positively regulated by activation transcription factor 3 (ATF3). Our study suggests that BEX4 plays a role in inhibiting tumor progression in ccRCC and maybe a new diagnostic and therapeutic target for ccRCC patients.

Dysregulation of deubiquitination contributes to various diseases, including cancer, and aberrant expression of deubiquitinating enzymes is involved in carcinoma progression. As a member of the ovarian tumor (OTU) deubiquitinases, OTUD4 is considered a tumor suppressor in many kinds of malignancies. The biological characteristics and mechanisms of OTUD4 in clear cell renal cell carcinoma (ccRCC) remain unclear. The downregulation of OTUD4 in ccRCC was confirmed based on the TCGA database and a validation cohort of 30-paired ccRCC and para-carcinoma samples. Moreover, OTUD4 expression was detected by immunohistochemistry in 50 cases of ccRCC tissues, and patients with lower levels of OTUD4 showed larger tumor size (p = 0.015). TCGA data revealed that patients with high expression of OTUD4 had a longer overall survival rate. In vitro and in vivo studies revealed that downregulation of OTUD4 was essential for tumor cell growth and metastasis in ccRCC, and OTUD4 overexpression inhibited these malignant phenotypes. We further found that OTUD4 sensitized ccRCC cells to Erastin-induced ferroptosis, and ferrostain-1 inhibited OTUD4-induced ferroptotic cell death. Mechanistic studies indicated that OTUD4 functioned as an anti-proliferative and anti-metastasic factor through the regulation of RNA-binding protein 47 (RBM47)-mediated activating transcription factor 3 (ATF3). OTUD4 directly interacted with RBM47 and promoted its stability via deubiquitination events. RBM47 was critical in ccRCC progression by regulating ATF3 mRNA stability, thereby promoting ATF3-mediated ferroptosis. RBM47 interference abolished the suppressive role of OTUD4 overexpression in ccRCC. Our findings provide mechanistic insight into OTUD4 of ccRCC progression and indicate a novel critical pathway OTUD4/RBM47/ATF3 may serve as a potential therapeutic pathway for ccRCC.

Abstract Background Ubiquitin-conjugating enzyme E2 N (UBE2N) is recognized in the progression of some cancers; however, little research has been conducted to describe its role in prostate cancer. The purpose of this paper is to explore the function and mechanism of UBE2N in prostate cancer cells. Methods UBE2N expression was detected in Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD) data, prostate cancer tissue microarrays, and prostate cancer cell lines, respectively. UBE2N knockdown or overexpression was used to analyze its role in cell viability and glycolysis of prostate cancer cells and tumor growth. XAV939 or Axin1 overexpression was co-treated with UBE2N overexpression to detect the involvement of the Wnt/β-catenin signaling and Axin1 in the UBE2N function. UBE2N interacting with Axin1 was analyzed by co-immunoprecipitation assay. Results UBE2N was upregulated in prostate cancer and the UBE2N-high expression correlated with the poor prognosis of prostate cancer. UBE2N knockdown inhibited cell viability and glycolysis in prostate cancer cells and restricted tumor formation in tumor-bearing mice. Wnt/β-catenin inhibition and Axin1 overexpression reversed the promoting viability and glycolysis function of UBE2N. UBE2N promoted Axin1 ubiquitination and decreased Axin1 protein level.

Abstract BACKGROUND Focal therapy for prostate cancer is rising. One of the actual challenge is the management of the margins. A real-time cancer diagnosis device could be a useful tool to control margins during focal therapy. Full Field Optical Coherence Tomography (FFOCT) is a recent technique to analyze tissue in real time. The aim of our study was to assess the accuracy of FFOCT in prostate cancer diagnosis on biopsy cores by urologists. METHODS 91 patients undergoing prostatic biopsies were included. Among these patients, we randomly selected 991 biopsy cores for the FFOCT analysis. FFOCT images were analyzed by two urologists and two urology residents, blinded for the results of the standard histological analysis (gold standard). The FFOCT analysis included the presence of prostate cancer, and clinically significant prostate cancer (ISUP≥2). Results were compared to the histological analysis. RESULTS All the 991 cores were analyzed. Among them, 236 cores (23,7%) were positive for prostate cancer and 37 cores (3,7%)for clinically significant prostate cancer (csPCa). Global accuracy was 86,9% for csPCa. Global negative predictive value (NPV) was 97,5% for csPCa. Reproducibility between readers was K= 0,46 (IC95%[0,37 – 0,48]). CONCLUSIONS Our results confirmed that FFOCT is feasible and accurate to eliminate prostate cancer on biopsy cores (NPV=97,5%). Further studies should evaluate FFOCT for framing biopsies during focal therapy procedures.

Metastasis is the greatest clinical challenge for UTUCs, which may have distinct molecular and cellular characteristics from earlier cancers. Herein, we provide single-cell transcriptome profiles of UTUC para cancer normal tissue, primary tumor lesions, and lymphatic metastases to explore possible mechanisms associated with UTUC occurrence and metastasis. From 28,315 cells obtained from normal and tumor tissues of 3 high-grade UTUC patients, we revealed the origin of UTUC tumor cells and the homology between metastatic and primary tumor cells. Unlike the immunomicroenvironment suppression of other tumors, we found no immunosuppression in the tumor microenvironment of UTUC. Moreover, it is imperative to note that stromal cells are pivotal in the advancement of UTUC. This comprehensive single-cell exploration enhances our comprehension of the molecular and cellular dynamics of metastatic UTUCs and discloses promising diagnostic and therapeutic targets in cancer-microenvironment interactions.

AbstractBackgroundRecurrent bladder cancer is the most common type of urinary tract malignancy; nevertheless, the mechanistic basis for its recurrence is uncertain. Innovative technologies such as single‐cell transcriptomics and spatial transcriptomics (ST) offer new avenues for studying recurrent tumour progression at the single‐cell level while preserving spatial data.MethodThis study integrated single‐cell RNA (scRNA) sequencing and ST profiling to examine the tumour microenvironment (TME) of six bladder cancer tissues (three from primary tumours and three from recurrent tumours).FindingsscRNA data‐based ST deconvolution analysis revealed a much higher tumour heterogeneity along with TME in recurrent tumours than in primary tumours. High‐resolution ST analysis further identified that while the overall natural killer/T cell and malignant cell count or the ratio of total cells was similar or even lower in the recurrent tumours, a higher interaction between epithelial and immune cells was detected. Moreover, the analysis of spatial communication reveals a marked increase in activity between cancer‐associated fibroblasts (CAFs) and malignant cells, as well as other immune cells in recurrent tumours.InterpretationWe observed an enhanced interplay between CAFs and malignant cells in bladder recurrent tumours. These findings were first observed at the spatial level.

The Rho/ROCK pathway regulates diverse cellular processes and contributes to the development and advancement of several types of human cancers. This study investigated the role of specific Rho GTPase-activating proteins (RhoGAP), ARHGAP6, in bladder cancer (BC). In this study, ARHGAP6 expression in BC and its clinical significance were investigated. In vitro and in vivo assays were used to explore the tumor‐related function and the underlying molecular mechanism ARHGAP6 of in BC. The mRNA and protein levels of ARHGAP6 significantly reduced in human BC tissues and cell lines compared with corresponding adjacent non-cancerous tissues and normal urothelial cells. In vitro, ARHGAP6 overexpression markedly decreased the viability, migration, and invasion of BC cells. Interestingly, low ARHGAP6 expression in BC strongly correlated with poor patient survival and was highly associated with metastasis and β-catenin signaling. Furthermore, ARHGAP6 expression strongly influenced the sensitivity of BC cells to mitomycin C treatment. Together, our results demonstrate that ARHGAP6 plays critical roles in regulating the proliferation, migration, invasion, and metastasis of BC cells possibly via the modulation of β-catenin and strongly influences the chemosensitivity of BC cells.

Objective: Deleted in liver cancer 1 (DLC1) is a GTPase-activating protein that is reported as a suppressor in certain human cancers. However, the detailed biological function of DLC1 is still unclear in human prostate cancer (PCa). In the present study, we aimed to explore the function of DLC1 in PCa cells.Methods: Silencing and overexpression of DLC1 were induced in an androgen-sensitive PCa cell line (LNCaP) using RNA interference and lentiviral vector transduction. The Cell Counting Kit-8 assay was performed to determine cell proliferation. The cell cycle was examined by perform-ing a propidium iodide staining assay.Results: Our results indicated that DLC1 overexpression markedly suppressed the proliferation and cell cycle progression of LNCaP cells. Moreover, DLC1 expression was negatively correlated with Rho-associated protein kinase (ROCK) expression in LNCaP cells. Importantly, this study showed that the ROCK inhibitor Y27632 restored the function of DLC1 in LNCaP cells and reduced the tumorigenicity of LNCaP cells in vivo.Conclusion: Our results indicated that DLC1 overexpression markedly suppressed the prolifer-ation and cell cycle progression of PCa cells and negatively correlated with ROCK expression in PCa cells and tissue.

Traditional Chinese medicine (TCM) is widely used as an alternative therapy for cancer treatment in China. Glutamine catabolism plays an important role in cancer development. Qici Sanling decoction (QCSL) suppresses bladder cancer growth. However, the association between QCSL and glutamine catabolism remains unknown. In this study, different doses of QCSL were applied to T24 cells, followed by the measurements of cell viability and apoptosis using CCK-8 and Annexin V/PI assay, respectively. Furthermore, glutamine consumption was detected using the glutamine assay kit. QCSL was observed to inhibit cell growth and induced cell apoptosis in a dose-dependent manner. Analysis of glutamine consumption revealed that QCSL suppressed glutamine consumption in T24 cells. Furthermore, QCSL decreased the mRNA and protein levels of c-Myc, GLS1, and SLC1A5. All these effects induced by QCSL could be alleviated by c-Myc overexpression, indicating c-Myc was involved in the protective role of QCSL in bladder cancer. In addition, QCSL was found to inhibit tumor growth in the xenograft tumor model. The similar results were obtained in tumor samples that protein levels of c-Myc, GLS1, and SLC1A5 were decreased upon treatment with QCSL. In conclusion, QCSL suppresses glutamine consumption and bladder cancer cell growth through inhibiting c-Myc expression.

Objective:To compare the efficacy and safety of transurethral thulium laser enucleation of prostate for benign prostatic hyperplasia (BPH) with laser controller and sheath.Methods:The clinical data of 128 BPH patients who underwent transurethral thulium laser enucleation of prostate (THuLEP) in our hospital from January to June 2020 were retrospectively analyzed. Prostatic enucleation by laser controller was performed in 66 patients (LC-THuLEP group). The prostatic urethral mucosa was cut into Ω shape at 0.5 cm in front of the verumontanum to expose the prostate capsule, and then the fiber was retracted into the laser controller. Push the gland directly between the prostate gland and the prostate surgical capsule and expand along the capsule by the laser controller. In case of bleeding or prostate adhesive cord, the fiber was extended to coagulate or cut off, and the prostate was eventually en bloc removed. THuLEP by sheath was performed in 62 cases (THuLEP group). The ages of patients in LC-THuLEP group and THuLEP group were (71.00±8.72) years and (70.32±7.80) years, respectively. The prostate volumes were (74.80±40.88) ml and (73.14±36.31) ml, respectively. Prostate specific antigen (PSA) was (4.67±4.99) ng/ml and (4.89±4.59) ng/ml, International Prostate Symptom Score (IPSS) was (19.48±5.30) points and (18.50±5.05) points, respectively. The quality of life (QOL) scores were (4.17 ± 0.78) points and (4.18± 0.67) points, the maximum urine flow rate (Q max) was (9.82± 2.58) ml /s and (9.98± 2.91) ml/s, respectively. Postvoid residual (PVR) was (60.20±39.19) ml and (61.11±52.83) ml, respectively. The international index of erectile function (IIEF-5) score was (5.58±4.50) and (5.60±4.16), respectively.There was no significant difference in preoperative baseline data between 2 groups ( P>0.05). The operation time, the reduced level of hemoglobin, the weight of removed tissue, The time to postoperative bladder irrigation, the time to indwelling catheter and complications were compared between the two groups. IPSS, QOL score, Q max, PVR, and complications were compared between the two groups at 1, 3 and 6 months after surgery, while IIEF-5 score were compared only at 6 months after surgery. Results:The operative time of LC-THuLEP group and THuLEP group was (71.85±25.68) min and (80.65±29.64) min, respectively, and the decrease of postoperative hemoglobin was (6.42±9.89) g/L and (9.47±10.79) g/L, respectively, the weight of the removed tissue was (56.73±31.21) g and (48.11±24.50) g, respectively, and the time to postoperative bladder irrigation was (14.73±2.71) h and (16.06±2.71) h, respectively, the time to indwelling catheter was (4.41±1.92)d and (4.31±1.66)d, respectively, with no statistically significant differences between the two groups. IPSS scores of LC-THuLEP group were (6.52±2.46) points, (5.83±2.43) points and (5.30±2.49) points at 1, 3 and 6 months after surgery, respectively. QOL scores were (2.36±0.85) points, (2.27±1.02) points and (1.98±0.77) points, Q max were (22.89±2.41) ml/s, (23.61±2.62) ml/s and (23.83±3.53) ml/s, respectively. In THuLEP group, IPSS were (7.60±1.89) points, (6.86±1.81) points and (6.44±1.78) points at 1, 3 and 6 months after surgery, and QOL scores were (2.68±0.67) points, (2.74±1.01) points and (2.35±0.68) points, respectively. Q max were (21.31±2.52) ml/s, (22.13±2.51) ml/s and (22.11±2.49) ml/s, respectively. Those indexes (except Qmax at 6 months)were better in LC-ThuLEP group than THuLEP group, and the differences were statistically significant ( P<0.05). PVR of LC-THuLEP group were (15.95±12.31) ml, (14.83±12.19) ml and (13.67±15.03) ml, respectively, PVR of THuLEP group were (21.89±21.14) ml, (20.03±21.51) ml and (19.69±21.19) ml, respectively, and there were no significant differences. There was no bladder injury, severe bleeding, blood transfusion or secondary operation. The incidence of urinary incontinence 1 month after surgery was 6.1% (4/66) in the LC-THuLEP group and 19.4% (12/62) in the THuLEP group, the difference was statistically significant ( P<0.05). There was no significant difference at 3 months (3/66 vs. 4/62) and 6 months (1/66 vs. 2/62) after surgery ( P>0.05). There were no significant differences in the incidence of epididymitis, urethral stricture and bladder neck contracture between the two groups ( P>0.05). Conclusion:Compared by sheath, THuLEP by laser controller could be a safe and effective surgical method with better curative effect and lower complication rate.

BACKGROUND In the pathogenesis and progression of prostate cancer, cell proliferation and cell migration results in tumor invasion and metastasis that is associated with patient morbidity and mortality. Rho-associated protein kinase (ROCK) has previously been shown to be upregulated in prostate cancer, but its biological role remains poorly understood. This study aimed to investigate the role of ROCK in the proliferation and migration of PC-3 and DU145 prostate cancer cells and to identify the possible targets involved by knockdown of ROCK1 and ROCK2 RNA expression. MATERIAL AND METHODS An RNA interference (RNAi) assay was performed to silence the expression of ROCK1 and ROCK2 in the PC-3 and DU145 human prostate cancer cell lines. Cells were also treated with a specific ROCK inhibitor, Y27632. A cell counting kit-8 (CCK-8) assay was used to determine the proliferation rate of prostate cancer cells, and cell migration and invasion assays were performed. Western blot and polymerase chain reaction were used to measure protein and RNA expression levels. RESULTS In PC-3 and DU145 prostate cancer cells, knockdown of ROCK1 and ROCK2 reduced cell migration and invasion. ROCK1 and ROCK2 regulated cell proliferation in PC-3 and DU145 prostate cancer cells. Protein levels of phosphorylated LIM kinase 1 (p-LIMK1) and matrix metalloproteinase-2 (MMP-2) were reduced in ROCK1 and ROCK2 siRNA transfected cells. CONCLUSIONS In PC-3 and DU145 human prostate cancer cells, ROCK promoted cell proliferation and migration by targeting LIMK1 and MMP-2.

Prostate cancer is one of the most common malignancies in men worldwide. Altered expression of ARHGAP10, a member of the Rho GTPase activating protein (RhoGAP) family, has been found in several human cancers. However, its clinical significance in prostate cancer remains unknown. In the current study, we found that mRNA levels of ARHGAP10 were significantly higher in prostate cancer tissues than in the non-cancerous controls. Gene set enrichment analysis (GSEA) revealed that ARHGAP10 expression was negatively correlated with the Wnt signaling pathway. Immunohistochemical staining results showed that 62.2% (56/90) and 65.5% (59/90) of prostate cancer tissues displayed low expression of ARHGAP10 and high expression of β-catenin, respectively. ARHGAP10 protein expression was significantly correlated with histologic grade (P < 0.0001), tumor stage (P = 0.0298), preoperative prostate specific antigen level (P = 0.0261), vital status (P = 0.0017) and β-catenin expression (P < 0.0001). Kaplan-Meier survival analysis indicated that patients with low levels of ARHGAP10 and high levels of β-catenin had poor overall survival. Multivariate analyses revealed that ARHGAP10 and β-catenin expression was independent prognostic factor for prostate cancer. In summary, the current study suggests that ARHGAP10 in association with β-catenin may play a role in the development of prostate cancer and serve as a prognostic factor for this disease.

Context: Bladder cancer, which has high recurrence, is one of the most deadly cancers in the world. Astragalus propinquus Schischkin (Fabaceae) and Sagittaria sagittifolia L. (Alismataceae) are important herbs reported to be effective in cancer therapy. Objective: The efficacy of QCSL (Qici Sanling decoction) in bladder cancer treatment was examined. Materials and methods: T24 cells were injected into the flanks of nude mice and the mice were randomly divided into five groups: control; 20 mg/kg XAV-939 (an inhibitor of the WNT/β-catenin pathway); QCSL (100, 200, or 400 mg/kg). After 7 weeks, the mice were anaesthetised using isoflurane and the xenografts were excised to perform further experiments. Results: Both XAV-939 (tumour volume: 379.67 ± 159.92 mm3) and QCSL (796.18 ± 101.6 mm3) dramatically suppressed tumour growth comparing with control group (3612.12 ± 575.03 mm3). XAV-939 and QCSL treatments decreased cell proliferation from 56.3 ± 0.05% to 29.02 ± 0.07% and 37.51 ± 0.04%, respectively. In agreement, more infiltration of immune cells and pyknotic cells upon XAV-939 (apoptosis rates: 43.92 ± 0.03%) and QCSL (34.57 ± 0.04%) treatment comparing with control group (15.59 ± 0.03%) were observed. Furthermore, TUNEL staining of xenograft tumours illustrated more apoptotic cells upon XAV-939 and QCSL treatment. Mechanistically, XAV-939 and QCSL treatments significantly inhibited WNT/β-catenin pathway in T24 xenograft tumours. Discussion and conclusions: Our findings give new insights into the role of QCSL in bladder cancer and explore potential mechanisms contributing to the therapeutic effects of QCSL in bladder cancer.

OBJECTIVE:To evaluate the effect of cefoxitin prophylactic in reducing the incidence of severe infection after transrectal prostate biopsy (TRPB).METHODS:This retrospective study included 155 cases of TRPB with a 5-day administration of oral levofloxacin at 200 mg bid (the control group) and another 167 cases with a 3-day administration of oral levofloxacin at the same dose plus intravenous cefoxitin at 2.0 g 2 hours before TRPB (the experimental group) according to the distribution characteristics of drug-resistance bacteria in our department. The patients of the control and experimental groups were aged (68.68 ± 8.12) and (68.72 ± 7.51) years, with PSA levels of (19.78 ± 21.57) and (21.15 ± 42.63) μg/L, involving (11.68 ± 1.44) and (11.77±1.02) biopsy cores, respectively. Comparisons were made between the two groups of patients in the incidence rate of severe infection, which was defined as lower urinary track symptoms plus the systemic inflammatory response syndrome (SIRS) within 7 days after TRPB.RESULTS:The incidence rate of postoperative severe infection was significantly lower in the experimental group than in the control (0.6% ［1/167］ vs 5.8% ［9/155］, P < 0.05). Blood cultures revealed positive E-coli strains in 6 cases in the control group, including 5 ESBL-positive and 4 quinolone-resistant and amikacin-sensitive cases, all sensitive to cefoxitin, cefoperazone/sulbactam and imipenem. The only one case of severe infection was shown to be negative in blood culture.CONCLUSIONS:Preoperative intravenous administration of cefoxitin according to the specific distribution characteristics of drug-resistance bacteria can significantly reduce the incidence of severe infection after TRPB.

Prostate cancer (PCa) is the second most common male cancer worldwide and the fifth leading cause of death from cancer in men. Early detection and risk stratification is the most effective way to improve the survival of PCa patients. Current PCa biomarkers lack sufficient sensitivity and specificity to cancer. Metabolite biomarkers are evolving as a new diagnostic tool. This review is aimed to evaluate the potential of metabolite biomarkers for early detection, risk assessment, and monitoring of PCa. Of the 154 identified publications, 27 and 38 were original papers on urine and serum metabolomics, respectively. Nuclear magnetic resonance (NMR) is a promising method for measuring concentrations of metabolites in complex samples with good reproducibility, high sensitivity, and simple sample processing. Especially urine-based NMR metabolomics has the potential to be a cost-efficient method for the early detection of PCa, risk stratification, and monitoring treatment efficacy.

OBJECTIVE:Solute carrier family 39, member 14 (SLC39A14), has been identified as a potential biomarker for various cancers. However, its roles in prostate cancer (PCa) are still unclear. The aim of this study was to investigate the clinical significance of SLC39A14 in patients with PCa and its functions in malignant phenotypes of PCa cells.PATIENTS AND METHODS:Subcellular localization and expression pattern of SLC39A14 protein were examined by immunohistochemistry. Then, the associations of SLC39A14 expression with various clinicopathological features and clinical outcome of patients with PCa were statistically evaluated. Subsequently, the effects of SLC39A14 overexpression and knockdown on PCa cell proliferation and motility were, respectively, examined by Cell Counting Kit-8, transwell, and wound-healing assays.RESULTS:The immunoreactive scores of SLC39A14 protein in human PCa tissues were significantly lower than those in normal prostate tissues. Based on the Taylor dataset, SLC39A14 downregulation occurred more frequently in patients with PCa with a higher Gleason score (P<0.001), advanced clinical stage (P=0.008), presence of metastasis (P=0.009), and prostate-specific antigen failure (P=0.006). More interestingly, the survival analysis identified SLC39A14 as an independent factor for predicting the biochemical recurrence-free survival of patients with PCa (P=0.017). Functionally, the enforced expression of SLC39A14 could suppress cell proliferation, invasion, and migration of PCa cell lines in vitro, which could be reversed by the knockdown of SLC39A14.CONCLUSION:Decreased expression of SLC39A14 may lead to malignant phenotypes of PCa cells and aggressive tumor progression in patients with PCa. Importantly, SLC39A14 may function as a tumor suppressor and a biomarker for screening patients with biochemical recurrence following radical prostatectomy.

Ras homolog gene family, member A (RhoA) has been reported as essential to the invasion process and aggressiveness of numerous cancers. However, there are only sparse data on the expression and activity of RhoA in clinically localised prostate cancer. In numerous cancers, tumour cells at the invasive front demonstrate more aggressive behaviour in comparison with the cells in the central regions. In the present study, the expression and activity of RhoA was evaluated in 34 paraffin-embedded and 20 frozen prostate tissue specimens obtained from 45 patients treated with radical prostatectomy for clinically localised cancer. The expression patterns of RhoA were assessed by immunohistochemical staining and western blotting. Additional comparisons were performed between the tumour centre, tumour front and distant peritumoural tissue. RhoA activity was assessed by G-LISA. Associations between RhoA expression and the clinical features and outcome of the patients were also analysed. The present study found an increasing gradient of expression from the centre to the periphery of index tumour foci. RhoA expression was significantly increased at the tumour front compared to the tumour centre, which was determined using immunohistochemistry (P= 0.001). Increased RhoA expression was associated with poor tumour differentiation in the tumour front (P= 0.044) and tumour centre (P= 0.039). Subsequent to a median follow-up period of 52 months, the rate of prostate-specific antigen (PSA) relapse was increased in patients with higher RhoA expression at the tumour front when compared with patients with lower RhoA expression (62.5 vs. 35.0%), although the difference was not significant (P= 0.09). There was no association between RhoA expression and the PSA level or pathological stage in the present study. In conclusion, RhoA expression was increased at the tumour front and was associated with poor tumour differentiation in the tumour front and tumour centre, indicating the potential role of RhoA in prostate cancer. RhoA expression may also act as a prognostic factor in prostate cancer. The present data provide a foundation for novel therapeutic approaches by targeting RhoA in prostate cancer.

目的 探讨经直肠超声前列腺穿刺活检联合墨水标记法病理诊断前列腺癌的应用价值.方法 2011年10月至2014年12月,137例患者因血清前列腺特异性抗原(PSA)升高在上海市周浦医院行前列腺穿刺活检.患者随机分两组,其中普通穿刺组68例,行常规经直肠超声引导前列腺穿刺活检;弹性超声组69例,行经直肠弹性超声前列腺穿刺活检联合墨水标记法病理标本,所有标本均按前列腺两侧叶矢状面尖部、中部、底部,前列腺两外侧面中部、底部以及经直肠弹性超声异常处穿刺l～3针.所有前列腺标本在采集后,在标本末端(外周带)标记上新鲜的黑色墨水后分别分装送病理,比较两组病理结果差异及对诊疗的影响.结果 普通穿刺组病理证实为前列腺癌24例,不典型增生6例,PIN 3例,前列腺增生35例.弹性超声组病理证实前列腺癌31例,不典型增生7例,PIN 6例,前列腺增生25例.弹性超声组前列腺癌检出率显著高于常规超声组(x=3.97,P＜0.05).两组共穿刺1 543针,其中外周带穿刺阳性者42例,中央带穿刺阳性者5例,外周带及中央带均阳性者8例.Gleason评分＞7分者11例,5分≤Gleason评分≤7分者40例,Gleason评分＜5分者4例.根据穿刺前列腺所处的位置行内分泌治疗者9例,前列腺癌根治术42例,经尿道前列腺电切术4例.结论 经直肠弹性超声前列腺穿刺活检联合墨水标记法有助于提高前列腺癌检出率,协助前列腺癌定位,对疾病的诊断以及手术方法的选择有着较高临床实用价值.