To characterize interstitial cystitis pathology based on the expression profile of urothelial tissue-specific master transcription factors.Bladder carcinoma cell lines derived from the urothelial stem cells (epithelial or mesenchymal) were used to identify candidate urothelial master transcription factors. Gene expression was measured with quantitative reverse transcription polymerase chain reaction. From the initial screening of 170 transcription factors (human homologs of Drosophila segmentation genes and known master transcription factors from a database), 28 transcription factors were selected. Subsequently, messenger ribonucleic acid from bladder biopsies of interstitial cystitis patients was purified, and gene expression levels of known urothelial marker genes and candidate master transcription factors were measured. Multivariate expression data were analyzed with spss software.Factor analysis decomposed the expression profile into four axes: principal axis 1 included retinoic acid receptors and 17 candidate master transcription factors. Principal axis 2 included KRT5 and five candidates. Principal axis 3 included transcription factor TP63 and two candidates. Principal axis 4 included SHH and two candidates. Principal component analysis segregated biopsies from Hunner's lesion in the principal component 1 (retinoic acid)/principal component 2 (SOX13)/principal component 3 (TP63) space.Urothelial master transcription factors could serve as novel diagnostic markers and potentially explain the molecular pathology of interstitial cystitis.
A 45-year-old woman was admitted to our hospital with a chief complaint of stress urinary incontinence. She had undergone simple hysterectomy due to myoma uteri at another hospital. X-ray examination and ultrasonography revealed a hydronephrosis on the right side after the surgery, which was improved immediately without intervention. She was diagnosed as having stress incontinence according to the history, findings of frequency/volume chart, 1-hour pad test, cystoscopy, drip infusion pyelography, magnetic resonance imaging and so on. Periurethral injection with non-animal stabilized hyaluronic acid/ dextranomer was performed. Incontinence was improved, but was not cured completely. After indigo carmine intravenous injection, cystoscopy was performed but no urine flow was noted from the right ureteral orfice. At the transvesical investigation, blue fluid was found at the vagina, and she then was diagnosed as having right ureterovaginal fistula. She underwent ureterovaginal fistula repair and reimplantation of the right ureter, and her incontinence was cured. To our knowledge, this is the first case of ureterovaginal fistula associated with stress incontinence.
Abstract The Rho family of GTPases are involved in actin cytoskeleton organization and associated with carcinogenesis and progression of human cancers. We investigated the roles of Rho family GTPases, prototypes RhoA, Rac1, and Cdc42, and the major downstream targets of RhoA, ROCK-I, and ROCK-II in testicular cancer. We quantified protein expression in paired tumor and nontumor samples from surgical specimens from 57 consecutive patients with testicular germ cell tumors using Western blotting. Protein expression of RhoA, ROCK-I, ROCK-II, Rac1, and Cdc42 was significantly higher in tumor tissue than in nontumor tissue (P < 0.0001). Expression of protein for RhoA, ROCK-I, ROCK-II, Rac1, and Cdc42 was greater in tumors of higher stages than lower stages (P < 0.0001, P < 0.001, P < 0.001, P < 0.0001, P < 0.0001, respectively). Within stage II nonseminoma (31 patients), protein levels of RhoA, ROCK-I, ROCK-II, Rac1, and Cdc42 in the primary tumor were lower in the group of 24 patients with no evidence of disease after therapy compared with 7 patients with disease that was refractory/recurrent (P < 0.05). Rho family GTPases may be involved in the progression of testicular germ cell tumors.
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