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We report a case of bladder diverticulum presumably caused by lower urinary tract dysfunction due to pelvic organ prolapse (POP) simultaneously treated with transurethral coagulation (TUC) of the bladder diverticulum and laparoscopic sacrocolpopexy (LSC). A literature search showed this is the first report of bladder diverticulum and POP surgically treated at the same time. A 71-year-old woman was referred to our hospital for the treatment of cystocele. She had both storage and voiding symptoms. She had a POPQ stage III cystocele and stage I uterine prolapse. Ultrasonography and computed tomographic scan showed a large volume of residual urine along with a bladder diverticulum. Since urodynamic studies revealed a low compliance bladder and obstruction, we opined that the lower urinary tract symptoms were induced by the cystocele. TUC of the bladder diverticulum and LSC were performed at the same time. After the operation, clean intermittent catheterization (CIC) was needed once a day for one month. Gradually, residual urine decreased and CIC became unnecessary. The bladder diverticulum disappeared, and there has been no recurrence of POP.

We report a case of left renal angiomyolipoma extending into the renal vein. A 67-year-old woman showed a left renal tumor which was 6 cm in diameter and had density equal to fat tissue in computed tomography. We suspected liposarcoma and performed radical nephrectomy and resection of thrombus. The pathological diagnosis was angiomyolipoma with no malignancy. To our knowledge, renal angiomyolipoma with tumor thrombus has been reported in 62 cases, and pulmonary embolism developed in 9 of these cases. We conclude that surgical treatment is effective in treating angiomyolipoma with tumor thrombus.

The p53 and EGFR pathways are frequently altered in bladder cancers, yet their contributions to its progression remain elusive. Here we report that DEAD box polypeptide 31 (DDX31) plays a critical role in the multistep progression of muscle invasive bladder cancer (MIBC) through its sequential interactions with mutant p53 (mutp53) and EGFR. In early MIBC cells, nuclear DDX31 bound mutp53/SP1 and enhanced mutp53 transcriptional activation, leading to migration and invasion of MIBC. Cytoplasmic DDX31 also bound EGFR and phospho-nucleolin (p-NCL) in advanced MIBC, leading to EGFR-Akt signaling activation. High expression of both cytoplasmic DDX31 and p53 proteins correlated with poor prognosis in patients with MIBC, and blocking the DDX31-NCL interaction resulted in downregulation of EGFR-Akt signaling, eliciting an in vivo anti-tumor effect against bladder cancer. These findings reveal that DDX31 cooperates with mutp53 and EGFR to promote progression of MIBC, and inhibition of DDX31-NCL formation may lead to potential treatment strategies for advanced MIBC.

Background: We assessed the change in LUTS after prostate brachytherapy to reveal factors for prolonged urination disorder. Materials and Methods: Four hundred and fourpatients received prostate brachytherapy at our institution and were followed-up for at least 2 years. We evaluated the correlation of mean IPSS changes and clinical factors. Using multivariate analysis, we also evaluated clinical factors with potential to delay IPSS resolution. Results: In cases with prostate volume more than 30 cm3, radiation dose to 90% of prostate volume (D90) more than 160 Gy, and radiation dose to 30% of the urethral volume (UD30) more than 240 Gy, mean IPSS levels were significantly higher, even 30 months after treatment. On multivariate analysis, baseline IPSS more than 8 points and D90 more than 160 Gy were significant predictors for delayed IPSS resolution. Conclusion: Our data suggest that higher baseline IPSS and higher D90 were predictors for prolonged urination disorder.

Background: Castration-resistant prostate cancer (CRPC)-related deaths are increasing worldwide. Therefore, clarification of the mechanisms of hormone-related tumor progression and resistance to anti-androgen drugs is useful in order to develop strategies for appropriate treatment of CRPC. Galectin-3 has been shown to be correlated with tumor progression in a variety of cancer types through the regulation of tumor proliferation, angiogenesis, and apoptosis. Materials and Methods: We examined tumor cell invasion and migration using the xCELLigence system. Control LNCaP and galectin- 3-expressing LNCaP (LNCaP-Gal-3) cells were cultured with androgen-depleted medium with 5% charcoal-stripped serum. Cells were treated for 24 h with or without dihydrotestosterone alone or combined with MDV3100 and bicalutamide; gene profile was then analyzed by microarray analysis and mRNA expression was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). We evaluated tumor growth using spheroids and xenograft tumor growth in a mouse model. Results: In vitro, LNCaP-Gal-3 cells promoted both cell migration and invasion in an androgen-independent manner compared to control LNCaP cells. Galectin-3 also enhanced anchorage-independent growth and xenograft tumor growth even after castration. Importantly, galectin-3 greatly enhanced transcriptional activity of the androgen receptor (AR), especially on treatment with dihydrotestosterone. In microarray and qRT-PCR analyses, galectin-3 increased the expression of several AR-target genes, such as kallikreinrelated peptidase 3 (KLK3), and transmembrane protease, serine 2 (TMPRSS2). These AR-target genes were not fully suppressed by anti-androgen drugs such as bicalutamide or MDV3100. Galectin-3 significantly inhibited the effect induced by anti-androgen drugs MDV3100 and bicalutamide, suggesting that galectin-3 may be involved in resistance to anti-androgen drug through enhancement of transcriptional activity of AR and expression of AR-related genes. Conclusion: These results suggest that galectin-3 is a potential target molecule for future treatment of anti-androgen drug-resistant prostate cancer.

A 66-year-old man with superficial bladder cancer was treated with transurethral resection (TURBT) in October 2011. The pathological diagnosis was urothelial carcinoma (UC), grade 2, T1. A second TURBT was performed one month later. The pathological diagnosis was UC, grade 3, T1. He was treated with intravesical bacillus Calmette-Guerin (BCG) after TURBT. His progress was satisfactory, but a small superficial bladder cancer was found on cystoscopy in August 2012. He was going to be treated with TURBT, but the serum alkaline phosphatase level was abnormally high on preoperative evaluation. Bone scintigraphy showed multiple bone metastases from non-muscle invasive bladder cancer (NMIBC) without local invasion. He was started on combined chemotherapy with 1, 000 mg/m2 gemcitabine on days 1, 8 and 15 and 70 mg/m2 cisplatin on day 2 every four weeks. He received denosumab for multiple bone metastases at the same time. Although he subsequently developed severe hypocalcemia, treatment was continued, and he completed four courses of chemotherapy. Bone scintigraphy and contrast-enhanced computed tomography showed reduction of the multiple bone metastases, and alkaline phosphatase decreased to the normal range. It is rare for NMIBC without local invasion to metastasize to other organs. Thus, it is necessary to consider distant metastases in patients with NMIBC.

A 61-year-old woman was referred to our department with a diagnosis of left solitary adrenal metastasis from cervical cancer in September 2011. She presented with postmenopausal bleeding in September 2010. The patient received seven courses of paclitaxel (175 mg/m2) and carboplatin (6 mg/GFR＋25) for stage IV cervical cancer with paraaortic, bilateral common iliac, mediastinal lymph node metastases and left adrenal metastasis from October 2010 to April 2011. Paraaortic radiation (50.4 Gy) was subsequently administered from May 2011 to July 2011. Abdominal nonenhanced computed tomography (CT) revealed a left 26×21 mm adrenal mass with regular margins (attenuation values 53 HU). On enhanced CT, the mass showed heterogeneous enhancement. F fluoro-2-deoxy D-glucose (FDG) positron emission tomography/CT images showed moderately increased FDG-avid uptake in the left adrenal tumor which was high enough to be suspicious of malignant tumor (standardized uptake value max : SUVmax 6.8). There were no other foci of pathologic uptake of FDG in the whole body. The plasma endocrinological examinations was all normal. Left laparoscopic adrenalectomy was performed. The final pathologic evaluation revealed adrenal cortical adenoma.

A 40-year-old woman was referred to our hospital because of pain extending from the left lateral abdomen to the left inferior limb. The abdominal computed tomography (CT) revealed an 8×7×12 cm retroperitoneal serous cystic mass. The serum carcinoembryogenic antigen (CEA) level was slightly elevated to 2.7 ng/ml. Therefore, we suspected it to be malignant, and we performed laparoscopic resection carefully. The retroperitoneal cyst was not adherent to the surrounding tissues and was easily dissected and removed under laparoscopy. Carbohydrale antigen (CA)19-9, CA125 and CEA levels in the fluid were elevated, but a cytology of the fluid was negative and no malignant sign was seen in the cyst wall. To our knowledge, this is the second reported case of retroperitoneal serous cyst resected by laparoscopic surgery in the Japanese literature.

Between January 1996 and December 2007, 111 patients with prostate cancer underwent radical prostatectomy, including 34 who received preoperative hormonal therapy. In this study, we reviewed 77 patients who did not undergo neoadjuvant hormonal therapy. The mean age was 65.5 years old and followup time was 40.7 months. The clinical stage was T1c in 60 patients, T2 in 16, and T3 in 1. Prostate specific antigen (PSA) at diagnosis ranged from 3.44 to 46.08 ng/ml (mean 10.18). At our institution, PSA failure after surgery was defined as PSA elevation above 0.2 ng/ml. The pathological stage was pT2 in 59 patients, pT3a in 11, pT3b in 7 and pN + (obturator lymph node) in none. The surgical margin was positive in 29.3% of the pT2 patients and 68.8% of the pT3 patients. Sixteen patients (20.8%) had PSA failure. PSA values at diagnosis and pathological T stage were significantly relevant to PSA failure. Patients with PSA failure underwent radiation therapy or hormonal therapy as a salvage adjuvant therapy. The PSA level was controlled well in majority of the patients. Only one patient died of cancer. In conclusion, 33 out of 111 patients who underwent radical prostatectomy had PSA failure. Sixteen of the 77 patients who were not given neoadjuvant therapy had PSA failure. The significant factors related to PSA failure were PSA values at diagnosis and pathological T stage., 過去12年間に111症例に根治的前立腺摘除術(手術時平均年齢65.5歳)を施行し、そのうち術前治療を行わなかった77症例について検討し、術後 PSA failureに関連する因子について検討した。術前PSAは平均10.18ng/ml、病理学的病期はpT2cが最も多かった(57.1%)。77例中術後PSA failureとなったのは16例(20.8%)で、追加治療として早期に外照射、内分泌治療を行った。平均観察期間は40.7ヵ月で、PSA failureは約20ヵ月まで起こっていた。PSA failureについて術前の患者背景や病理学的因子との相関を検討したところ、対象77例においてPSA failureと相関があったのは診断時のPSA値、pathological T stageであり、診断時のPSAが高いほど有意にPSA failureは多くなった。臨床病期はpT2、pT3a、pT3bの3群におけるPSA failure free survivalでは、pTが進むにつれて有意にPSA failureを起こした。以上より、患者背景とPSA failureは診断時のPSAとpT stageが相関していた。

腹腔鏡下尿管切石術を施行した3症例を報告した。症例1は73歳男, 症例2は34歳男, 症例3は34歳男で, 全例extracorporeal shock wave lithotripsy(ESWL), TUL等を施行されたが難治性であり, 切石術を希望していた。3例とも腹腔鏡下尿管切石術の適応とされるlarge stone, impacted stone, stone situated in the upper ureter or over the pelvic brimを満たしていた。症例1では結石は尿管と同側の腎盂内の2ヶ所にあり, 尿管結石摘除後にそのままポートから軟性尿管鏡を挿入し, 尿管切開部から腎盂内にアプローチした。鉗子で腎盂内の結石もそのまま摘出でき, 体位変換も必要なく, 尿管操作も容易であった。尿管切開は結石の直上で, 症例1ではスピッツメスの刃を持針器で把持して切開した。症例2, 3はロティキュレーターエンドミニシアーズを使用して, 尿管の切開を尿管と平行に行うことができた。この器具は2ヶ所で屈曲させることができ, 自由な方向から正確に切開可能であった。3例とも安全に手術を終え, 術後経過良好であった。, With the development of extracorporeal shock wave lithotripsy (ESWL), improved endourologic instrumentation, and medical dissolution therapy, the need for open ureterolithotomy has become less common. Open operation is occasionally necessary when less invasive techniques fail. As in many of the surgical specialties, laparoscopy has become more common in urologic surgery. We recently experienced three cases of ureteral stones, which were treated by laparoscopic ureterolithotomy. The stones were all large and impacted stones. The patients were a 73-year-old man and two 34-year-old men. All procedures were performed by a retroperitoneal approach. We used Roticulator endo mini-shears resourcefully, when we incised the ureteral wall. After surgery, all three patients were stone-free, and hydronephrosis was improved.

OBJECTIVES To clarify the invasive mechanisms of muscle-invasive bladder cancer (BCa) would be useful for the determination of appropriate treatment strategies.We previously showed that hepatocyte growth factor (HGF)-MET signaling is correlated with invasiveness of BCa cells. Here, we investigated the effects of the MET inhibitor, cabozantinib (XL184), on BCa cells. METHODS We first conducted Western blot analysis to investigate MET expression in BCa cell lines. Next, we examined the effect of cabozantinib on their proliferation and invasive abilities using MTT and Matrigel invasion assays, respectively. Invasion assays were performed using the xCELLigence system. Additionally, to investigate the biological function of HGF-MET signaling, we analyzed gene expression profiles and performed real-time polymerase chain reaction analyses of 5637 cells that were cultivated with or without HGF stimulation, with or without cabozantinib. RESULTS MET was highly expressed in 4 of 5 BCa cell lines, and 5637 and T24 cells showed especially high protein expression of MET. Cabozantinib suppressed cell proliferation and invasion (cell index; mock, 1.49 vs HGF, 2.26 vs HGF + XL184, 1.47, P < .05). Gene expression profile analysis indicated that matrix metalloproteinase 1 (MMP1) was significantly elevated at the mRNA level with addition of HGF. Moreover, cabozantinib suppressed HGF-induced MMP1 expression in 5637 T24 cells. CONCLUSIONS These data indicate that cabozantinib suppressed MMP1 expression by blocking HGF-MET signaling and that HGF-MET-MMP1 signaling is involved in the invasiveness and proliferation of BCa cells. These results suggest that cabozantinib might prove useful for future treatment of muscleinvasive BCa.