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[AUGMENTED ONLAY BUCCAL MUCOSAL GRAFT URETEROPLASTY FOR URETERAL STRICTURE: A CASE REPORT].
Nihon Hinyokika Gakkai Zasshi
January 2025
Department of Urology, Keio University School of Medicine.
A 14-year-old boy developed hydronephrosis and worsening renal function due to fibroepithelial polyps of the bladder and left ureter at the age of 12 years. The endoscopic treatment of ureteral polyps was attempted by his previous doctor; however urethral stricture and ureteral stricture developed and was untreatable. Therefore, he was referred to our hospital for further reconstructive treatment.
View Article and Find Full Text PDF« Augmented radiotherapy » in the management of high-risk prostate cancer (PCa): a systematic review.
Crit Rev Oncol Hematol
January 2025
Centre de Radiothérapie Charlebourg, La Défense, Groupe Amethyst, 65, avenue Foch, 92250 La Garenne-Colombes, France; Department of radiation oncology, Institut Bergonié, Bordeaux, France.
Background: In patients with high-risk (HR) prostate cancer (PCa) treated with radiotherapy and androgen deprivation therapy (ADT), intensification with androgen receptor pathway inhibitor (ARPI) improves overall survival (OS), at the cost of significant side-effects. We hypothesized that "augmented RT" schedules (defined as either dose-escalation on the prostate gland over 78Gy and/or addition of whole pelvic radiotherapy (WPRT)), combined with long-term ADT can reach excellent prostate cancer specific survival (PCSS) in this population with little detrimental impact on quality of life.
Methods: We searched Pubmed database until February 8, 2024.
An Acellular Platform to Drive Urinary Bladder Tissue Regeneration.
Adv Ther (Weinh)
January 2025
Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Division of Pediatric Urology, Department of Surgery, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL 60611, USA; Center for Regenerative Nanomedicine, Northwestern University, Chicago, IL 60611, USA; Department of Biomedical Engineering, McCormick School of Engineering, Northwestern University, Evanston, IL 60208, USA.
Impaired bladder compliance secondary to congenital or acquired bladder dysfunction can lead to irreversible kidney damage. This is managed with surgical augmentation utilizing intestinal tissue, which can cause stone formation, infections, and malignant transformation. Co-seeded bone marrow mesenchymal stem cell (MSC)/CD34+ hematopoietic stem cell (HSPC) scaffolds (PRS) have been successful in regenerating bladder tissue.
View Article and Find Full Text PDFMetabolic consequences and tubular function after augmentation cystoplasty in children with neurogenic bladder.
J Chin Med Assoc
September 2024
Faculty of Medicine, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, ROC.
Background: Many studies have reported the renal outcomes and metabolic consequences after augmentation cystoplasty (AC), however few studies have discussed changes in renal tubular function. The aim of this study was to determine the prevalence of metabolic disturbances, evaluate renal tubular function and 24-hour urine chemistry to evaluate the association between metabolic alterations and urolithiasis after AC.
Methods: We investigated serum biochemistry, blood gas, and 24-hour urinary metabolic profile of children who underwent AC between January 2000 and December 2020.
Loss of Kmt2c or Kmt2d primes urothelium for tumorigenesis and redistributes KMT2A-menin to bivalent promoters.
Nat Genet
January 2025
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Members of the KMT2C/D-KDM6A complex are recurrently mutated in urothelial carcinoma and in histologically normal urothelium. Here, using genetically engineered mouse models, we demonstrate that Kmt2c/d knockout in the urothelium led to impaired differentiation, augmented responses to growth and inflammatory stimuli and sensitization to oncogenic transformation by carcinogen and oncogenes. Mechanistically, KMT2D localized to active enhancers and CpG-poor promoters that preferentially regulate the urothelial lineage program and Kmt2c/d knockout led to diminished H3K4me1, H3K27ac and nascent RNA transcription at these sites, which leads to impaired differentiation.
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