scholarly journals Urine Cytology and Commercially Available Urine-Based Markers for Monitoring of Bladder Urothelial Carcinoma

2007 ◽  
Vol 38 (1) ◽  
pp. 48-52
Author(s):  
Jose A. Karam ◽  
Yair Lotan ◽  
Shahrokh F. Shariat
2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e17018-e17018
Author(s):  
Ario Takeuchi ◽  
Masaki Shiota ◽  
Junichi Inokuchi ◽  
Masatoshi Eto

e17018 Background: Second transurethral resection (TUR), which is now recommended for all T1 high-grade bladder urothelial carcinoma, may not be necessary for patients with minimal tumor burden at the first TUR. T1 microstaging by the recognition of the muscularis mucosae or vascular plexus may be one promising method for evaluating tumor burden, but is sometimes technically difficult to assess. The number of TUR chips with tumor invading into lamina propria (T1chips) is easy to assess and can be available for all patients with T1 bladder urothelial carcinoma. Our aim was to determine clinicopathological factors which can predict the existence of residual tumor on the second TUR specimens for T1 high-grade bladder urothelial carcinoma. Methods: A total of 50 patients were diagnosed with T1 high-grade bladder urothelial carcinoma after the first TUR. We performed second TUR for the 50 patients. The median interval from the first and the second TUR was 6 week (range, 2-10). Voided urine cytology was taken in all patients between the first and the second TUR, at least 1 week after the first TUR. The existence of proper muscle tissue was confirmed in all specimens for the first and the second TUR. Tumor size, the number of tumor, the presence of carcinoma in situ (CIS), the number of TUR chips containing lamina propria invasion (T1chips) were recorded for the first TUR specimens. Results: A total of 20 (40%) patients had residual tumor on the second TUR. The second TUR stage was: T0 30 (60%); Ta/is 7 (14%); T1 9 (18%); and T2 4 (8%), respectively. In univariate analysis, positive urine cytology before the first TUR (48% vs 0% in negative), positive urine cytology between the first and second TUR (76% vs 21% in negative), and multiple T1 chips on the first TUR specimens (58% vs 6% in one T1 chip) were associated with residual tumor on the second TUR. In addition, in multivariate analysis, the number of T1 chips on the first TUR and urine cytology between the first and the second TUR were the significant predictors for residual tumor on the second TUR. Of 15 patients with multiple T1 chips and positive urine cytology between the first and the second TUR, 13 (87%) had residual tumor on the second TUR, compared to 0% (0/15) in those with one T1 chip and negative urine cytology between the first and the second TUR. Conclusions: Second TUR may not be necessary for all patients with T1 high-grade bladder urothelial carcinoma. The number of T1 chips on the first TUR and urine cytology between the first and the second TUR are useful factors for predicting second TUR stage.


2021 ◽  
Author(s):  
Chien-Feng Li ◽  
Ti-Chun Chan ◽  
Cheng-Tang Pan ◽  
Pichpisith Pierre Vejvisithsakul ◽  
Jia-Chen Lai ◽  
...  

2021 ◽  
Author(s):  
Meredith M. Nichols ◽  
Jordan P. Reynolds ◽  
Jesse K. McKenney ◽  
Marlo M. Nicolas ◽  
Patrick J. McIntire ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dexin Shen ◽  
Yayun Fang ◽  
Fenfang Zhou ◽  
Zhao Deng ◽  
Kaiyu Qian ◽  
...  

Abstract Background CDCA3 is an important component of the E3 ligase complex with SKP1 and CUL1, which could regulate the progress of cell mitosis. CDCA3 has been widely identified as a proto-oncogene in multiple human cancers, however, its role in promoting human bladder urothelial carcinoma has not been fully elucidated. Methods Bioinformatic methods were used to analyze the expression level of CDCA3 in human bladder urothelial carcinoma tissues and the relationship between its expression level and key clinical characteristics. In vitro studies were performed to validate the specific functions of CDCA3 in regulating cell proliferation, cell migration and cell cycle process. Alterations of related proteins was investigated by western blot assays. In vivo studies were constructed to validate whether silencing CDCA3 could inhibit the proliferation rate in mice model. Results Bioinformatic analysis revealed that CDCA3 was significantly up-regulated in bladder urothelial carcinoma samples and was related to key clinical characteristics, such as tumor grade and metastasis. Moreover, patients who had higher expression level of CDCA3 tend to show a shorter life span. In vitro studies revealed that silencing CDCA3 could impair the migration ability of tumor cells via down-regulating EMT-related proteins such as MMP9 and Vimentin and inhibit tumor cell growth via arresting cells in the G1 cell cycle phase through regulating cell cycle related proteins like p21. In vivo study confirmed that silencing CDCA3 could inhibit the proliferation of bladder urothelial carcinoma cells. Conclusions CDCA3 is an important oncogene that could strengthen the migration ability of bladder urothelial carcinoma cells and accelerate tumor cell growth via regulating cell cycle progress and is a potential biomarker of bladder urothelial carcinoma.


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