Treated History of Noninvasive Grade 1 Transitional Cell Carcinoma

Prout, George R.; Barton, Bruce; Griffin, Pamela P.; Friedell, Gilbert H.

doi:10.1016/s0022-5347(17)36924-0

Cited by 191 publications

(123 citation statements)

References 32 publications

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“…Superficial tumors, corresponding to 70% of the cases, are typically papillary and confined to the urothelial mucosa (stage Ta) or to the lamina propria (stage T1) (Haukaas et al, 1999). Apart from displaying a high risk of recurrent disease, most superficial tumors are of low grade (G1 or G2), rarely progress, and are associated with a highly favorable prognosis (Prout et al, 1992;Haukaas et al, 1999). In contrast, high-grade Ta tumors (TaG3), and T1 tumors, represent a significant risk of future tumor progression and death from the disease (Herr, 2000).…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of early-stage bladder carcinomas by expression profiles, FGFR3 mutation status, and loss of 9q

et al. 2006

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We used gene expression profiling, mutation analyses of FGFR3 and TP53, and LOH analyses of chromosome 9 and the TP53 region on chromosome arm 17p, to molecularly characterize 75 Ta and T1 bladder carcinomas. We identified four major cellular processes related to cell cycle, protein synthesis, immune response, and extra cellular components that contribute to the expressional heterogeneity of early-stage urothelial cell carcinoma (UCC). Activating FGFR3 mutations were found at the highest frequency in G1 tumors (80%), and showed a strong correlation with FGFR3 expression. In contrast, G3 tumors displayed mutations in less than 10% of the cases and a low level of FGFR3 expression. Even though LOH on chromosome 9 was not associated with any specific expression pattern, our data indicate that loss of chromosome 9 is associated with tumor development rather than initiation. The combined analyses suggest the existence of two types of UCC tumors, one which is characterized by FGFR3 mutation or expression, high expression of protein synthesis genes, and low expression of cell cycle genes. Furthermore, the presented data underscore FGFR3 receptor involvement in urothelial cell transformation as the presence of FGFR3 mutations has a major impact on the global gene expression profile of bladder carcinomas.

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Section: Introductionmentioning

confidence: 99%

Molecular characterization of early-stage bladder carcinomas by expression profiles, FGFR3 mutation status, and loss of 9q

et al. 2006

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“…Previous studies have shown the importance of genetic alterations affecting known oncogenes and tumour suppressor genes (Knowles, 1999). An increase in grade, characterised by a loss of differentiation, and the presence of dysplasia as well as tumour multiplicity are determinants of poor prognosis (Heney, 1992;Prout et al, 1992). Studies using microsatellites, and more recently, array-based comparative genomic hybridisation, have shown that loss of heterozygosity (LOH) especially loss of chromosome 9 is a frequent finding in early stage bladder cancer (Cairns et al, 1993;Ruppert et al, 1993;Keen and Knowles, 1994;Primdahl et al, 2002).…”

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confidence: 99%

Gene expression profiling of noninvasive primary urothelial tumours using microarrays

et al. 2005

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At present, the mechanism leading to bladder cancer is still poorly understood, and our knowledge about early events in tumorigenesis is limited. This study describes the changes in gene expression occurring during the neoplastic transition from normal bladder urothelium to primary Ta tumours. Using DNA microarrays, we identified novel differentially expressed genes in Ta tumours compared to normal bladder, and genes that were altered in high-grade tumours. Among the mostly changed genes between normal bladder and Ta tumours, we found genes related to the cytoskeleton (keratin 7 and syndecan 1), and transcription (high mobility group AT-hook 1). Altered genes in high-grade tumours were related to cell cycle (cyclin-dependent kinase 4) and transcription (jun d proto-oncogene). Furthermore, we showed the presence of high keratin 7 transcript expression in bladder cancer, and Western blotting analysis revealed three major molecular isoforms of keratin 7 in the tissues. These could be detected in urine sediments from bladder tumour patients.

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“…the tumour is confined to the lamina propria, the disease represents a major therapeutic challenge and a continuous threat to the patients since the tumours recur after transurethral resection of the primary in more than 70% of the cases Thompson et al, 1993). In addition, progression to more advanced stages and/or grades occurs in 16Ð25% of the cases (Prout et al, 1992).…”

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confidence: 99%

Cytogenetic monoclonality in multifocal uroepithelial carcinomas: evidence of intraluminal tumour seeding

et al. 1999

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Summary Twenty-one multifocal urinary tract transitional cell carcinomas, mostly bladder tumours, from a total of six patients were processed for cytogenetic analysis after short-term culturing of the tumour cells. Karyotypically related, often identical, cytogenetically complex clones were found in all informative tumours from each case, including the recurrent tumours. Rearrangement of chromosome 9, leading to loss of material from the short and/or the long arm, was seen in all cases, indicating that this is an early, pathogenetically important event in transitional cell carcinogenesis. The presence of related clones with great karyotypic similarity in anatomically distinct tumours from the same bladder indicates that multifocal uroepithelial tumours have a monoclonal origin and arise via intraluminal seeding of viable cancer cells shed from the original tumour. Later lesions may develop also from cells shed from the so called second primary tumours. The relatively complex karyotypes seen in all lesions from most cases argue that the seeding of tumour cells is a late event that succeeds the acquisition by them of multiple secondary genetic abnormalities.

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Treated History of Noninvasive Grade 1 Transitional Cell Carcinoma

Cited by 191 publications

References 32 publications

Molecular characterization of early-stage bladder carcinomas by expression profiles, FGFR3 mutation status, and loss of 9q

Molecular characterization of early-stage bladder carcinomas by expression profiles, FGFR3 mutation status, and loss of 9q

Gene expression profiling of noninvasive primary urothelial tumours using microarrays

Cytogenetic monoclonality in multifocal uroepithelial carcinomas: evidence of intraluminal tumour seeding

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