Examination of Tumorigenesis of Precursor Lesions in Bladder Cancer by in situ Hybridization

Krause, Steffen; Feil, G.; Beiter, Thomas; Preßler, H.; Schrott, K. M.; Bichler, K.-H.

doi:10.1159/000075964

Cited by 8 publications

(4 citation statements)

References 22 publications

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“…Our study showed a higher percentage of polysomic cells in urothelial dysplasia compared with reactive atypia (p = 0.001). DNA cytometry showed increasing aneuploidy relative to the degree of dysplasia in flat urothelial lesions,25 but the present study and previous studies26 also highlight the difficulty of distinguishing histologically overlapping lesions (CIS versus dysplasia, dysplasia versus reactive atypia). This study shows a significant difference of mean values of polysomy in these lesions, albeit individual cases cannot be attributed to the above-mentioned lesion types exclusively based on multitarget FISH analysis.…”

Section: Discussioncontrasting

confidence: 46%

Value of multicolour fluorescence in situ hybridisation (UroVysion) in the differential diagnosis of flat urothelial lesions

Schwarz

Rechenmacher

Filbeck³

et al. 2007

J Clin Pathol

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Section: Discussioncontrasting

confidence: 46%

Value of multicolour fluorescence in situ hybridisation (UroVysion) in the differential diagnosis of flat urothelial lesions

Schwarz

Rechenmacher

Filbeck³

et al. 2007

J Clin Pathol

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“…The present study and previous studies reported by Krause et al (2004) and Schwarz et al (2008) also highlight the difficulty of distinguishing histologically overlapping lesions (CIS vs. dysplasia, dysplasia vs. reactive atypia). This study shows a significant difference in the mean values of polysomy in these lesions.…”

Section: Discussionsupporting

confidence: 73%

Detection of chromosomal instability in preneoplastic flat lesions and conditions of the urinary bladder using UroVysion fluorescence in-situ hybridization

Elsayed¹

2015

Egyptian Journal of Pathology

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Detection of chromosomal instability in preneoplastic flat lesions and conditions of the urinary bladder using UroVysion fluorescence in-situ hybridization Walid S.H. ElsayedPurpose Identification of genetic alterations in preneoplastic lesions to frank cancer helps in elucidating the progression of these genetic changes. The aim of the present study was to identify chromosomal imbalance using UroVysion fluorescence in-situ hybridization in patients with various preneoplastic flat lesions and conditions in routine paraffin-embedded bladder biopsy samples.Materials and methods A total of148 paraffin-embedded tissue blocks from 75 patients with preneoplastic flat lesions and conditions [hyperplasia, reactive atypia, dysplasia, carcinoma in situ (CIS), squamous metaplasia, intestinal metaplasia, and control] were analyzed using tissue sections hybridized with centromeric probes for chromosomes 3, 7, and 17 and a locus-specific probe 9p21 for detecting cytogenetic abnormalities.Results Polysomy of at least one of the chromosomes was found in more than 90% of samples in CIS and invasive bladder tumors, whereas it was found in 80% of samples in dysplasia. The mean percentage of polysomic cells in flat urothelial hyperplasia, reactive urothelial atypia, intestinal metaplasia, keratinizing squamous metaplasia, and histologically normal urothelium in patients with tumors ranged from 11 to 20%, whereas in CIS and dysplasia it was 69 and 49%, respectively. Deletion of the P16 locus was most frequently observed in aneuploid lesions.Conclusion Detection of chromosomal imbalance with UroVysion fluorescence in-situ hybridization is a useful method for the detection of genetically unstable preneoplastic flat lesions and conditions, and can help in resolving difficult cases, particularly in the differential diagnosis of reactive atypia and dysplasia. Moreover, evaluation of ongoing genetic instability might provide additional insight into urinary bladder cancer risk assessment beyond that of the location and histology of the premalignant lesion. Egypt J Pathol 35:157-162 c Comparison of flat urothelial hyperplasia (1), squamous metaplasia (2), intestinal metaplasia (3), dysplasia (4), and carcinoma in situ (5) as regards histology (a) and fluorescence in-situ hybridization signals (b).Chromosomal instability in preneoplastic flat lesions Elsayed 159

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“…Human genes causing cytokinesis failure have been involved in cancer pathogenesis [ 74 , 75 ], inducing the formation of polyploid cells with an abnormal growth. In particular, this is true for bladder cancer [ 76 ]. Aneuploidy may be a consequence, among other possibilities, of the centrosome function impairment.…”

Section: Resultsmentioning

confidence: 99%

Contextualizing the Genes Altered in Bladder Neoplasms in Pediatric and Teen Patients Allows Identifying Two Main Classes of Biological Processes Involved and New Potential Therapeutic Targets

Porrello

Piergentili

2015

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Research on bladder neoplasms in pediatric and teen patients (BNPTP) has described 21 genes, which are variously involved in this disease and are mostly responsible for deregulated cell proliferation. However, due to the limited number of publications on this subject, it is still unclear what type of relationships there are among these genes and which are the chances that, while having different molecular functions, they i) act as downstream effector genes of well-known pro- or anti- proliferative stimuli and/or interplay with biochemical pathways having oncological relevance or ii) are specific and, possibly, early biomarkers of these pathologies. A Gene Ontology (GO)-based analysis showed that these 21 genes are involved in biological processes, which can be split into two main classes: cell regulation-based and differentiation/development-based. In order to understand the involvement/overlapping with main cancer-related pathways, we performed a meta-analysis dependent on the 189 oncogenic signatures of the Molecular Signatures Database (OSMSD) curated by the Broad Institute. We generated a binary matrix with 53 gene signatures having at least one hit; this analysis i) suggests that some genes of the original list show inconsistencies and might need to be experimentally re- assessed or evaluated as biomarkers (in particular, ACTA2) and ii) allows hypothesizing that important (proto)oncogenes (E2F3, ERBB2/HER2, CCND1, WNT1, and YAP1) and (putative) tumor suppressors (BRCA1, RBBP8/CTIP, and RB1-RBL2/p130) may participate in the onset of this disease or worsen the observed phenotype, thus expanding the list of possible molecular targets for the treatment of BNPTP.

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Examination of Tumorigenesis of Precursor Lesions in Bladder Cancer by in situ Hybridization

Cited by 8 publications

References 22 publications

Value of multicolour fluorescence in situ hybridisation (UroVysion) in the differential diagnosis of flat urothelial lesions

Value of multicolour fluorescence in situ hybridisation (UroVysion) in the differential diagnosis of flat urothelial lesions

Detection of chromosomal instability in preneoplastic flat lesions and conditions of the urinary bladder using UroVysion fluorescence in-situ hybridization

Contextualizing the Genes Altered in Bladder Neoplasms in Pediatric and Teen Patients Allows Identifying Two Main Classes of Biological Processes Involved and New Potential Therapeutic Targets

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