Previous studies have found that tumor-associated macrophages (TAMs) promote cancer progression. We previously reported that TAMs promote prostate cancer metastasis via activation of the CCL2–CCR2 axis. The CCR4 (receptor of CCL17 and CCL22) expression level in breast cancer was reported to be associated with lung metastasis. The aim of this study was to elucidate the role of CCR2 and CCR4 in prostate cancer progression. CCR2 and CCR4 were expressed in human prostate cancer cell lines and prostate cancer tissues. In vitro co-culture of prostate cancer cells and macrophages resulted in increased CCL2 and CCR2 levels in prostate cancer cells. The addition of CCL2 induced CCL22 and CCR4 production in prostate cancer cells. The migration and invasion of prostate cancer cells via enhanced phosphorylation of Akt were promoted by CCL17 and CCL22. CCR4 may be a potential candidate for molecular-targeted therapy.

Priapism is defined as a persistent and painful erection lasting longer than four hours without sexual stimulation. Based on episode history and pathophysiology, priapism is classified into three subtypes: ischemic (low-flow), non-ischemic (high-flow), and stuttering priapism. Ischemic priapism is characterized by a persistent, painful erection with remarkable rigidity of the corpora cavernosa caused by a disorder of venous blood outflow from this tissue mass, and is similar to penile compartment syndrome. Stuttering priapism is characterized by a self-limited, recurrent, and intermittent erection, frequently occurring in patients with sickle cell disease. Non-ischemic priapism is characterized by a painless, persistent nonsexual erection that is not fully rigid and is caused by excess arterial blood flow into the corpora cavernosa. Because ischemic and non-ischemic priapism differ based on emergency status and treatment options, appropriate discrimination of each type of priapism is required to initiate adequate clinical management. The goal of management of priapism is to achieve detumescence of the persistent penile erection and to preserve erectile function after resolution of the priapism. To achieve successful management, urologists should address this emergency clinical condition. In the present article, we review the diagnosis and clinical management of the three types of priapism.

BACKGROUND:The authors elucidated an etiologic role of human papillomavirus (HPV) infection in carcinoma of the bladder. METHODS: One hundred seventeen of 224 patients with bladder carcinoma who were treated between 1997 and 2009 were enrolled in this study. The presence of HPV DNA was tested on frozen carcinoma tissues that were obtained by transurethral resection using a polymerases chain reaction-based method. Localization of HPV was observed on archival tissue specimens by in situ hybridization (ISH) for high-risk HPV DNA. Cyclin-dependent kinase (CDK) inhibitor 2A (inhibits CDK4) (p16-INK4a) and minichromosome maintenance protein-7 (mcm-7)-surrogate markers for high-risk HPV-E7 oncoprotein-and HPV-L1 (capsid) protein expression were evaluated by immunohistochemistry. RESULTS: HPV types 16, 18, 31, 33, 52, and 58, and an unknown HPV type were detected in 18 of 117 samples (15%) from patients with bladder carcinoma. HPV16 was identified in 6 samples, HPV18 was identified in 4 samples, and HPV33 was identified in 3 samples. All were single HPV type infections. HPV was detected in 38% (12 of 28) of histologic grade 1 bladder carcinomas, 8.5% (6 of 71) of grade 2 bladder carcinomas, and in 0% (0 of 18) of grade 3 bladder carcinomas. Multivariate analysis indicated that younger age (<60 years; odds ratio [OR], 10.9; 95% confidence interval [CI], 2.6-45.3) and grade 1 tumors (OR, 4.5; 95% CI, 1.2-17.0) were associated with HPV infection. ISH analysis indicated that high-risk HPV DNA was localized in the nuclei of tumor cells of all HPV-positive samples. p16-INK4a and mcm-7 were expressed in 94% and 89% of HPV-positive carcinoma cells, respectively. HPV-L1 protein expression, which suggested reproductive HPV infection, was not observed in any carcinoma. CONCLUSIONS: The current results indicated that high-risk HPV is likely to be a causative agent of some low-grade bladder carcinomas that develop in younger patients.

The status of human papillomavirus (HPV) infection in urothelial inverted papilloma was examined in the present study. Formalin-fixed and paraffin-embedded tissues from eight cases of inverted papilloma of the bladder were studied. The presence of HPV-DNA was examined by modified GP5/6+PCR using archival tissue sections by microdissection. HPV genotype was determined with a Hybri-Max HPV genotyping kit. Immunohistochemical analysis for p16-INK4a, mcm7, HPV-E4, and L1, and in situ hybridization (ISH) for the HPV genome were performed. HPV was detected in 7 of 8 cases (87.5%) of inverted papilloma. Three cases were diagnosed as inverted papilloma with atypia, while the remaining 5 were typical cases. HPV-18 was detected in two cases, including one inverted papilloma with atypia, and HPV-16 was detected in four cases, including one inverted papilloma with atypia. Multiple HPV type infection was detected in one typical case and one atypical case. High-risk HPV was present in all HPV-positive cases. Cellular proteins, p16-INK4a and mcm7, which are surrogate markers for HPV-E7 expression, were detected in all HPV-positive cases, and their levels were higher in inverted papilloma with atypia than in typical cases. In contrast, HPV-E4 and L1, which are markers for HPV propagation, were observed in some parts of the typical inverted papilloma tissue. High-risk HPV infection may be one of the causes of urothelial inverted papilloma, and inverted papilloma with atypia may have malignant potential.

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Objectives:To investigate the prevalence of human papillomavirus (HPV) in the genital and urinary tract of men with urethritis. Methods: Cell samples were collected from the penis, urethra and urine of 142 men with urethritis. A HPV test was performed on the samples using the modified GP5+/6+ polymerase chain reaction method , and the HPV genotype was determined using a HPV GenoArray test. Results: Out of 142 urethritis patients, HPV was detected in 48% (68 cases), and high-risk HPV was found in 32% (46 cases) of patients, on their penis or in the urinary tract (urethra or urine). HPV was detected in 31% in the penis, 20% in the urethra and 24% in the urine, while high-risk HPV was identified in 23% in the penis, 12% in the urethra and 11% in the urine. Among the HPV-positive men, 66% had HPV infection in the urinary tract where the most common HPV types were HPV6, HPV16, HPV18 and HPV58. Single HPV-type infection was more frequently found in the urinary tract (89%) than in the penis (65%) (P < 0.05). Conclusions: Similar to the penis, the urinary tract represents a common HPV infection site in men with urethritis.

Understanding the mechanism of lymph node metastasis, a poor prognostic sign for prostate cancer, and the further dissemination of the disease is important to develop novel treatment strategies. Recent studies have reported that C‐C chemokine receptor 7 (CCR7), whose ligand is CCL21, is abundantly expressed in lymph node metastasis and promotes cancer progression. Tumor necrosis factor‐α (TNF‐α) is chronically produced at low levels within the tumor microenvironment. The aim of this study was to determine whether TNF‐α promotes prostate cancer dissemination from metastatic lymph nodes through activation of the CCL21/CCR7 axis. First, human prostate cancer cells were determined to express both TNF‐α and CCR7. Second, low concentrations of TNF‐α were confirmed to induce CCR7 in prostate cancer cells through phosphorylation of ERK. Finally, CCL21 was found to promote the migration of prostate cancer cells through phosphorylation of the protein kinase p38. Our results suggest that TNF‐α leads to the induction of CCR7 expression and that the CCL21/CCR7 axis might increase the metastatic potential of prostate cancer cells in lymph node metastasis.

Aims To evaluate urinary incontinence using the International Consultation on Incontinence Questionnaire‐Short Form (ICIQ‐SF), daily pad use, and 24‐h pad weight test before and after radical prostatectomy (RP) chronologically, and the correlation between them. Methods ICIQ‐SF and questions on daily pad use provided subjective, and 24‐h pad weight test for objective evaluation. Results In total, 258 cases were recruited. The continence rate at 12 months after RP was 67% for no pad use, 87% for security 1 pad/day, and 94% for 1 pad/day. The median ICIQ‐SF total score before and at 1, 3, 6, and 12 months after RP was 0, 10, 7, 5, and 4, respectively. Incontinence patterns differed when comparing ICIQ‐SF results pre‐ and post‐RP. Significant correlation existed between the ICIQ‐SF total score, 24‐h pad weight test, and daily pad use; however, point distribution on each scatter plot varied widely. Comparing results before and at 12 months after RP revealed complete recovery for 35% of patients from the ICIQ‐SF total score, 67% from daily pad use, and 64% from the 24‐h pad weight test. A combination of all 3 showed a recovery of preoperative levels in 29% of patients. Conclusions ICIQ‐SF was effective and convenient for evaluating UI, including the pattern of UI, after RP. Significant correlation, but wide variations, among ICIQ‐SF, daily pad use, and the 24‐h pad weight test existed. The best evaluation method would be the one that can compare UI status pre‐ and post‐RP using the ICIQ‐SF and 24‐h pad weight test.