Robot-assisted radical cystectomy for bladder cancer after low anterior resection: A case report.

Radical cystectomy after low anterior resection is rare, and no cases of robotic surgery have been reported. Cystectomy in patients who have undergone a previous pelvic surgery, whether open or endoscopic, requires caution to avoid damaging other organs due to anatomical changes caused by adhesions in a limited space. Additionally, the curative nature of the treatment must be maintained.

An optimal method of hydrogel spacer insertion for stereotactic body radiation therapy of prostate cancer.

Purpose: This study aimed to explore an ideal method for hydrogel spacer insertion by analyzing the efficacy and safety of our originally developed apex expansion method.

Materials And Methods: Overall, 100 patients with low- and intermediate-risk localized prostate cancer treated with stereotactic body radiation therapy were included. A hydrogel spacer was inserted in 64 and 36 patients using the conventional and apex expansion methods, respectively.

Distribution analysis of hydrogel spacer and evaluation of rectal dose reduction in Japanese prostate cancer patients undergoing stereotactic body radiation therapy.

Background: To report on our primary experience with the placement of a hydrogel spacer following stereotactic body radiation therapy (SBRT) in low- and intermediate-risk prostate cancer patients and assess its impact on dosimetry as well as acute toxicity.

Methods: A total of 70 patients treated with SBRT (total dose of 36.25 Gy) in 5 fractions were included.

[PREDICTIVE FACTORS OF THE INITIAL TREATMENT FOR 207 BLUNT RENAL TRAUMA CASES BASED ON THE CLASSIFICATION FOR RENAL INJURY OF JAPANESE ASSOCIATION FOR THE SURGERY OF TRAUMA 2008's VERSION].

(Objective) We retrospectively investigated the applicability of the Japanese Association for the Surgery of Trauma (JAST) classification version 2008 for renal injuries as predictive factors of the initial treatment for 207 blunt renal injury cases. (Materials and methods) We reviewed 207 patients between 1982 and 2013 who were admitted to our institution with blunt renal trauma. Patients were classified as conservative management group, immediate transcatheter arterial embolization (TAE) group, and immediate nephrectomy group by initial treatment.

MUC1-C oncoprotein induces TCF7L2 transcription factor activation and promotes cyclin D1 expression in human breast cancer cells.

MUC1 is a heterodimeric glycoprotein that is overexpressed in breast cancers. The present studies demonstrate that the oncogenic MUC1 C-terminal subunit (MUC1-C) associates with the TCF7L2 transcription factor. The MUC1-C cytoplasmic domain (MUC1-CD) binds directly to the TCF7L2 C-terminal region.

MUC1-C oncoprotein regulates glycolysis and pyruvate kinase M2 activity in cancer cells.

Aerobic glycolysis in cancer cells is regulated by multiple effectors that include Akt and pyruvate kinase M2 (PKM2). Mucin 1 (MUC1) is a heterodimeric glycoprotein that is aberrantly overexpressed by human breast and other carcinomas. Here we show that transformation of rat fibroblasts by the oncogenic MUC1-C subunit is associated with Akt-mediated increases in glucose uptake and lactate production, consistent with the stimulation of glycolysis.

Inhibition of the MUC1-C oncoprotein induces multiple myeloma cell death by down-regulating TIGAR expression and depleting NADPH.

The MUC1-C oncoprotein is aberrantly expressed in most multiple myeloma cells. However, the functional significance of MUC1-C expression in multiple myeloma is not known. The present studies demonstrate that treatment of multiple myeloma cells with a MUC1-C inhibitor is associated with increases in reactive oxygen species (ROS), oxidation of mitochondrial cardiolipin, and loss of the mitochondrial transmembrane potential.

Dependence on the MUC1-C oncoprotein in non-small cell lung cancer cells.

Non-small cell lung cancer (NSCLC) cells are often associated with constitutive activation of the phosphoinositide 3-kinase (PI3K) → Akt → mTOR pathway. The mucin 1 (MUC1) heterodimeric glycoprotein is aberrantly overexpressed in NSCLC cells and induces gene signatures that are associated with poor survival of NSCLC patients. The present results show that the MUC1 C-terminal subunit (MUC1-C) cytoplasmic domain associates with PI3K p85 in NSCLC cells.

MUC1-C oncoprotein promotes STAT3 activation in an autoinductive regulatory loop.

Signal transducer and activator of transcription 3 (STAT3) is activated in human breast cancer and other malignancies. Mucin 1 (MUC1) is a heterodimeric cell surface glycoprotein that is overexpressed in human carcinomas and, like STAT3, promotes cell survival and induces transformation. We found that in breast cancer cells, the MUC1 carboxyl-terminal receptor subunit (MUC1-C) associates with the gp130-Janus-activated kinase 1 (JAK1)-STAT3 complex.

Terminal differentiation of chronic myelogenous leukemia cells is induced by targeting of the MUC1-C oncoprotein.

Chronic myelogenous leukemia (CML) is caused by expression of the Bcr-Abl fusion protein in hematopoietic stem cells. The MUC1-C oncoprotein is expressed in CML blasts and stabilizes Bcr-Abl. The present studies demonstrate that treatment of KU812 and K562 CML cells with GO-201, a cell-penetrating peptide inhibitor of MUC1-C oligomerization, downregulates Bcr-Abl expression and inhibits cell growth.

Survival of human multiple myeloma cells is dependent on MUC1 C-terminal transmembrane subunit oncoprotein function.

The MUC1 C-terminal transmembrane subunit (MUC1-C) oncoprotein is a direct activator of the canonical nuclear factor-kappaB (NF-kappaB) RelA/p65 pathway and is aberrantly expressed in human multiple myeloma cells. However, it is not known whether multiple myeloma cells are sensitive to the disruption of MUC1-C function for survival. The present studies demonstrate that peptide inhibitors of MUC1-C oligomerization block growth of human multiple myeloma cells in vitro.

Potent cytotoxic effect of a novel nuclear factor-kappaB inhibitor dehydroxymethylepoxyquinomicin on human bladder cancer cells producing various cytokines.

Objectives: To explore the potential therapeutic effects of the nuclear factor-kappaB (NF-kappaB) inhibitor dehydroxymethylepoxyquinomicin (DHMEQ). KU-19-19 cells, originally derived from a patient with invasive bladder cancer who exhibited marked leukocytosis, produce multiple cytokines. This model of clinically advanced bladder cancer, in which NF-kappaB is constitutively activated, was used in this study.

[Primary small cell carcinoma of the ureter: a case report].

An 84-year-old female was referred to our hospital to be examined for left hydronephrosis. Abdominal pelvic computed tomography and ureteroscopy showed an obstructing mass in the left ureter. A biopsy of the mass revealed the presence of small cell carcinoma.

Tumour length of the largest focus predicts prostate-specific antigen-based recurrence after radical prostatectomy in clinically localized prostate cancer.

Objective: To investigate the possible significance of tumour dimensional variables, including maximum tumour diameter (MTD), maximum tumour area (MTA) and total tumour volume (TTV), with standard prognostic factors for predicting prostate-specific antigen (PSA) recurrence after radical prostatectomy (RP).

Patients And Methods: Serial whole sections of the prostate from 164 patients who had RP for localized prostate cancer were investigated. Cox proportional hazards regression models were used for univariate and multivariate analyses to test the relationships between biochemical failure and clinicopathological factors, including tumour dimensional variables.

Angiotensin II type 1 receptor antagonist enhances cis-dichlorodiammineplatinum-induced cytotoxicity in mouse xenograft model of bladder cancer.

Objectives: To examine whether candesartan enhances the cytotoxicity of cis-dichlorodiammineplatinum (CDDP) in mice with bladder cancer as a method to enhance the therapeutic effects of CDDP. CDDP is an antitumor agent conventionally used against bladder cancer; however, its therapeutic efficacy appears to not be fully satisfactory. Recent studies have shown the antitumor activity of the angiotensin II type 1 receptor antagonist candesartan.

Brachytherapy with permanent seed implantation.

Permanent interstitial brachytherapy with iodine-125 (I-125) or palladium 103 (Pd-103) seeds is a common treatment option in the United States, and numerous articles on outcomes after long-term follow up have been published. With the treatment's apparent high efficacy and low morbidity, permanent seed implantation has become the most frequently employed procedure for localized prostate cancer and has replaced radical prostatectomy. Even taking into account the good features of the treatment, the performance of permanent seed implantation in Japan had not been allowed because of the country's strict laws on radiation safety.

Comparison of intraoperative ultrasound with postimplant computed tomography--dosimetric values at Day 1 and Day 30 after prostate brachytherapy.

Purpose: To compare the results of intraoperative dosimetry with those of postimplant computed tomography (CT)-based dosimetry after (125)I prostate brachytherapy.

Methods And Materials: We treated 412 prostate cancer patients with (125)I prostate brachytherapy, with or without external beam radiotherapy at our institution. Neoadjuvant hormone therapy was administered to 331 patients (80.

Effect of angiotensin II type 1 receptor antagonist on tumor growth and angiogenesis in a xenograft model of human bladder cancer.

Several authors have investigated the antitumor activity of angiotensin II type 1 receptor (AT1R) antagonists, which are widely used as antihypertensive drugs. In this study, we evaluated the efficacy of the AT1R antagonist candesartan against bladder cancer. For the study in vitro, human bladder cancer cells (KU-19-19) were cultured with and without angiotensin II (A II) and candesartan, and cell viability and vascular endothelial growth factor (VEGF) secretion were analyzed.

Rectal morbidity following I-125 prostate brachytherapy in relation to dosimetry.

Background: To investigate rectal morbidity after I-125 prostate brachytherapy and to analyze predictive factors of rectal morbidity.

Methods: A group of 227 consecutive patients with localized prostate cancer were treated with I-125 prostate brachytherapy with or without external beam radiotherapy (EBRT) between September 2003 and January 2005. Rectal morbidity (diarrhea, bleeding and pain) was evaluated using the Radiation Therapy Oncology Group (RTOG) criteria.

[Influence of androgen deprivation therapy on prostate volume in patients with prostate cancer undergoing prostate brachytherapy with permanent seed implantation].

Objective: Enlarged prostate often causes pubic arch interference during needle insertion on transperineal interstitial permanent prostate brachytherapy. Pre-treatment hormonal therapy is necessary for downsizing the prostate gland in such cases. The degree of prostate downsizing with anti-androgen treatment before iodine 125 permanent seed implant brachytherapy and its relation to clinical as well as pathological parameters were assessed.

Angiotensin II type 1 receptor antagonist candesartan as an angiogenic inhibitor in a xenograft model of bladder cancer.

Purpose: There have been several studies on the antitumor activity of angiotensin II type 1 receptor (AT1R) antagonists. In this study, we evaluated the efficacy of the AT1R antagonist candesartan in bladder cancer.

Experimental Design: For the study in vitro, human bladder cancer cells (KU-19-19) were cultured with or without angiotensin II and candesartan.

[Neuroendocrine differentiation in adenocarcinoma of the prostate with progression of disease during hormonal treatment: a report of two cases].

Prostatic neuroendocrine (NE) carcinoma is a rare situation and the NE differentiation in the prostate adenocarcinoma appears to be characterized as poor prognosis, rapid tumor progression and the androgen-independent state, for which there is currently no successful therapy. We report two cases of NE differentiated prostatic carcinoma, which were diagnosed adenocarcinoma initially and the tumors progressed universally with NE differentiation during androgen suppression therapy.