Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677481 (urinary frequency)
 1,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a rare case of plasmacytoid urothelial carcinoma (PUC) of the urinary bladder. A 50-year-old man complained of pollakiuria and urinary incontinence. MRI detected a bladder tumor invading the rectum and bilateral hydroureteronephrosis. Radical cystectomy with partial resection of the rectum was performed, and ileus due to peritoneal dissemination occurred 2 years after surgery. He died of the disease 42 months after the initial presentation. Histologically, urothelial carcinoma in situ with a focal invasive urothelial carcinoma (IUC) component and widely spread PUC was observed. There was no lymph node metastasis. PUC cells had eccentrically placed nuclei and eosinophilic cytoplasm resembling plasmacytoma cells, and proliferated with a single-cell infiltrative pattern to the outside of the bladder. IUC cells with intracytoplasmic lumina were focally intermingled with PUC cells. Immunohistochemically, PUC cells were positive for cytokeratin 7, epithelial membrane antigen, and CA19-9, but negative for cytokeratin 20, E-cadherin, p63, and lymphoid markers. The Ki-67 labeling index of PUC cells was 9.3%. IUC containing intracytoplasmic lumina showed intermediate features of conventional IUC and PUC morphologically and immunohistochemically. PUC is a distinct entity of bladder cancer with a high propensity for invasion and poor prognosis.
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PMID:Plasmacytoid urothelial carcinoma of the urinary bladder: a case report and immunohistochemical study. 1904 Nov 93

Benign prostatic hyperplasia (BPH) is linked to lower urinary tract symptoms (LUTS) such as incomplete bladder emptying, urinary frequency and urgency. Mechanisms responsible for BPH are not fully known. Here, we tested whether beta-catenin (CTNNB1) immunostaining intensity and distribution differ in human glandular BPH tissue specimens compared to normal prostate tissue. Multiplex immunostaining of CTNNB1, its putative transcriptional target gene lymphoid enhancer binding factor 1 (LEF1), and the epithelial marker E-cadherin were examined in clinical human prostate specimens with or without histological BPH (pure epithelial or mixed stromal-epithelial nodules). BPH specimens were obtained from 24 men who experienced LUTS and underwent transurethral resection of the prostate surgery. Control specimens were tumor-adjacent histologically normal prostate tissue from 48 patients who underwent radical prostatectomy. The resulting multispectral images were unmixed and optical densities recorded to quantify staining abundance, cellular (membranous, cytoplasmic, and nuclear) and tissue localization (stromal versus epithelial), and determination of percentage of CTNNB1-positive cells. The following CTNNB1 indices were significantly higher in BPH compared to normal prostate tissue: overall staining intensity, staining intensity in prostate stromal cell membranes, cytoplasm and nuclei, and prostate epithelial cell nuclei. The following LEF1 indices were significantly lower in BPH compared to tumor-adjacent normal prostate tissue: stromal LEF1 staining intensity, percentage of LEF1-positive stromal cells, and intensity of LEF1 staining in stromal cell membranes, cytoplasm, and nuclei. The percentage of stromal cells with CTNNB1(+)/LEF1(-) nuclei was higher and percentage of stromal cells with CTNNB1(-)/LEF1(+) nuclei was lower in BPH compared to tumor-adjacent normal prostate tissues. These results support the hypothesis that CTNNB1 expression increases in specific BPH tissue compartments. Further, since nuclear LEF1 staining does not coincide with cytoplasmic or nuclear CTNNB1 staining, it does not appear to be a reliable index of CTNNB1 activity in adult human prostate.
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PMID:Beta-catenin is elevated in human benign prostatic hyperplasia specimens compared to histologically normal prostate tissue. 2560 77

Interstitial cystitis/bladder pain syndrome (IC/BPS) is a heterogeneous syndrome which is usually characterized by urinary frequency, nocturia, and bladder pain. Several pathomechanisms have been proposed, including uroepithelial dysfunction, mast cell activation, neurogenic inflammation, autoimmunity, and occult urinary tract infections. It is possible that an inflammatory process alters regulation of urothelial homeostasis and results in dysfunction of the bladder epithelium. Different phenotypes of IC/BPS have been explored including Hunner and non-Hunner type IC, hypersensitive bladder, and bladder pain both with and without functional somatic syndrome. Different gene expressions have also been found in different IC phenotypes. Abnormal expressions of uroplakin, chondroitin sulfate and adhesive protein E-cadherin, tight junction protein zonula occludens-1 in IC/BPS bladder suggest abnormal epithelial differentiation in this bladder disease. Analysis of inflammatory proteins, or cytokines in the urine or serum provides another diagnostic foundation forIC/BPS subtypes. The involvement of IC/BPS in systemic functional somatic syndrome and other pelvic organ diseases might also subdivide subtypes of IC/BPS. Chronic inflammation, increased urothelial apoptosis, and abnormal urothelial function are closely associated in IC bladders. This article reviews recent research on the pathomechanisms of IC, which might help us in mapping the heterogeneity of the disease.
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PMID:Pathomechanism of Interstitial Cystitis/Bladder Pain Syndrome and Mapping the Heterogeneity of Disease. 2791 72