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      Plasmacytoid Urothelial Carcinoma of the Urinary Bladder

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          Abstract

          Plasmacytoid urothelial carcinoma (PUC) of the bladder is a rare histologic variant. We retrospectively analyzed a large series of bladder PUC from a single institution.

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          The cell-cell adhesion molecule E-cadherin.

          F Van Roy, G. Berx (2008)
          This review is dedicated to E-cadherin, a calcium-dependent cell-cell adhesion molecule with pivotal roles in epithelial cell behavior, tissue formation, and suppression of cancer. As founder member of the cadherin superfamily, it has been extensively investigated. We summarize the structure and regulation of the E-cadherin gene and transcript. Models for E-cadherin-catenin complexes and cell junctions are presented. The structure of the E-cadherin protein is discussed in view of the diverse functions of this remarkable protein. Homophilic and heterophilic adhesion are compared, including the role of E-cadherin as a receptor for pathogens. The complex post-translational processing of E-cadherin is reviewed, as well as the many signaling activities. The role of E-cadherin in embryonic development and morphogenesis is discussed for several animal models. Finally, we review the multiple mechanisms that disrupt E-cadherin function in cancer: inactivating somatic and germline mutations, epigenetic silencing by DNA methylation and epithelial to mesenchymal transition-inducing transcription factors, and dysregulated protein processing.
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            ICUD-EAU International Consultation on Bladder Cancer 2012: Screening, diagnosis, and molecular markers.

            Ashish Kamat, Paul K. Hegarty, Jason R. Gee … (2013)
            To present a summary of the 2nd International Consultation on Bladder Cancer recommendations on the screening, diagnosis, and markers of bladder cancer using an evidence-based strategy. A detailed Medline analysis was performed for original articles addressing bladder cancer with regard to screening, diagnosis, markers, and pathology. Proceedings from the last 5 yr of major conferences were also searched. The major findings are presented in an evidence-based fashion. Large retrospective and prospective data were analyzed. Cystoscopy alone is the most cost-effective method to detect recurrence of bladder cancer. White-light cystoscopy is the gold standard for evaluation of the lower urinary tract; however, technology like fluorescence-aided cystoscopy and narrow-band imaging can aid in improving evaluations. Urine cytology is useful for the diagnosis of high-grade tumor recurrence. Molecular medicine holds the promise that clinical outcomes will be improved by directing therapy toward the mechanisms and targets associated with the growth of an individual patient's tumor. The challenge remains to optimize measurement of these targets, evaluate the impact of such targets for therapeutic drug development, and translate molecular markers into the improved clinical management of bladder cancer patients. Physicians and researchers eventually will have a robust set of molecular markers to guide prevention, diagnosis, and treatment decisions for bladder cancer. Copyright © 2012 European Association of Urology. All rights reserved.
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              RB1 in cancer: different mechanisms of RB1 inactivation and alterations of pRb pathway in tumorigenesis.

              G Tesoriere, Renza Vento, Riccardo Di Clemente … (2013)
              Loss of RB1 gene is considered either a causal or an accelerating event in retinoblastoma. A variety of mechanisms inactivates RB1 gene, including intragenic mutations, loss of expression by methylation and chromosomal deletions, with effects which are species-and cell type-specific. RB1 deletion can even lead to aneuploidy thus greatly increasing cancer risk. The RB1gene is part of a larger gene family that includes RBL1 and RBL2, each of the three encoding structurally related proteins indicated as pRb, p107, and p130, respectively. The great interest in these genes and proteins springs from their ability to slow down neoplastic growth. pRb can associate with various proteins by which it can regulate a great number of cellular activities. In particular, its association with the E2F transcription factor family allows the control of the main pRb functions, while the loss of these interactions greatly enhances cancer development. As RB1 gene, also pRb can be functionally inactivated through disparate mechanisms which are often tissue specific and dependent on the scenario of the involved tumor suppressors and oncogenes. The critical role of the context is complicated by the different functions played by the RB proteins and the E2F family members. In this review, we want to emphasize the importance of the mechanisms of RB1/pRb inactivation in inducing cancer cell development. The review is divided in three chapters describing in succession the mechanisms of RB1 inactivation in cancer cells, the alterations of pRb pathway in tumorigenesis and the RB protein and E2F family in cancer. Copyright © 2013 Wiley Periodicals, Inc.
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                Author and article information

                Journal
                Title: American Journal of Clinical Pathology
                Publisher: Oxford University Press (OUP)
                ISSN (Print): 0002-9173
                ISSN (Electronic): 1943-7722
                Publication date Created: May 2017
                Publication date Created: May 01 2017
                Publication date Created: March 23 2017
                Publication date (Print): May 2017
                Publication date (Print): May 01 2017
                Publication date (Electronic): March 23 2017
                Volume: 147
                Issue: 5
                Pages: 500-506
                Article
                DOI: 10.1093/ajcp/aqx029
                PubMed ID: 28371875
                SO-VID: f901d362-ff50-4e17-9ecb-88257892ff7a
                Copyright © © 2017
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