Chromosomal Aberrations Associated With Invasion in Papillary Superficial Bladder Cancer

Simon, Ronald; Bürger, Horst; Brinkschmidt, Christian; Böcker, W.; Hertle, L.; Terpe, Hans-Joachim

doi:10.1016/s0022-5347(05)68640-5

Cited by 45 publications

(76 citation statements)

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“…In a study of chromosomal aberrations by comparative genomic hybridisation, there was a very small percentage of gains of 11q13 in pTa tumours. However, in pT1 tumours, loss of chromosome 11 was observed with the exception of 11q13 which was often gained or amplified (Simon et al, 1998). In this study, c-myc and CCND1 may be dysfunctional due to the observed increased copy number, and it is possible that Genetics and Genomics PP=progressed at presentation, patients with 5pT2 at initial diagnosis; RP=recurrer progressors, patients with pTa/pT1 disease at initial diagnosis who subsequently recurred and progressed with their disease; amp=gene amplification.…”

Section: Discussionmentioning

confidence: 63%

Genetic aberrations of c-myc and CCND1 in the development of invasive bladder cancer

et al. 2002

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Detrusor muscle invasive transitional cell carcinoma is associated with poor prognosis and is responsible for the majority of bladder cancer related deaths. Amplifications of c-myc and CCND1 are associated with detrusor-muscle-invasive transitional cell carcinoma, however, their precise role in driving disease progression is unclear. Fluorescence in situ hybridisation on archival tissue from 16 patients with primary diagnosis of 5pT2 transitional cell carcinoma and 15 cases with primary pTa/pT1 disease subsequently progressing to detrusor-muscle-invasion was performed, in the latter group both pre and post muscle invasive events were studied. No patients presenting with 5pT2 had amplification of c-myc, two out of 16 (12.5%) had CCND1 amplification. Of patients who developed 5pT2, two out of 15 (13.3%) had amplification of c-myc, both in 5pT2, five out of 15 (33.3%) had CCND1 amplification, two in pTa/pT1 tumours, three in 5pT2 transitional cell carcinomas. In total, two out of 31 (6.5%) of patients' 5pT2 TCCs were amplified for c-myc and six out of 31 (19%) were amplified for CCND1. Eighty-seven per cent (40 out of 46) of tumours were polysomic for chromosome 8 and 80% (37 out of 46) were polysomic for chromosome 11 and this reflected the high copy numbers of c-myc and CCND1 observed. In almost all cases an increase in c-myc/CCND1 copy number occurred prior to invasion and persisted in advanced disease. Amplification of CCND1 or alterations in c-myc/CCND1 early in bladder cancer may have clinical relevance in promoting and predicting progression to detrusor-muscle-invasive transitional cell carcinoma.

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Section: Discussionmentioning

confidence: 63%

Genetic aberrations of c-myc and CCND1 in the development of invasive bladder cancer

et al. 2002

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“…These findings indicate significant genetic differences between these two UC tumor stages, although they are grouped together as "superficial tumors." 6,7 Second, gains and amplifications generally predominate over deletions in advanced-stage UC, suggesting that tumor suppressor genes are inactivated in early stages, and activation of oncogenes is more likely to come into play in more advanced stages of UC progression. 6 -8 The most common genomic hot spots are summarized in Table 1.…”

Section: "Hot Spots" In the Urothelial Bladder Carcinoma Genomementioning

confidence: 99%

“…Loss of 9q is the earliest genetic event in pTa tumors and covers 5 major deleted regions (9q11-13, 9p22-23, 9q12-13, 9q21-22, and 9q34), suggesting that 1 or several tumor suppressor genes may be located in those regions and may be responsible for early-stage UC. 6 Several investigators have concluded that distinct losses and/or gains of genetic material may have an impact on tumor behavior and patient prognosis. A significant association has been proposed between gains of 5p and an increased risk of tumor progression in a subset of pT1 tumors.…”

Section: "Hot Spots" In the Urothelial Bladder Carcinoma Genomementioning

confidence: 99%

Genetic alterations in urothelial bladder carcinoma

Mhawech‐Fauceglia

Cheney

Schwaller

2006

Cancer

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New oncogenes and tumor suppressor genes that play an important role in the pathogenesis of urothelial bladder carcinoma have been discovered. The objectives of this review were to summarize the most important oncogenes and tumor suppressor genes involved in urothelial carcinoma and to address their role in pathogenesis, their prognostic value, and their potential use as therapeutic targets.The collected data led the authors to propose a common pathway in which the fibroblastic growth factor receptor 3 (FGFR3) mutation seems to be the earliest genetic abnormality responsible for the transformation from normal tissue to atypia and dysplasia. Three different progression pathways were proposed: The first operative pathway is from dysplasia to superficial papillary pathologic Ta

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“…In addition to these known hotspots of chromosomal copy number changes in prostatic adenocarcinoma, a novel region of chromosomal loss on 4q could be detected in our subset of cases. Deletions on 4q are frequent events in other tumour entities such as lung tumours (Petersen et al, 1997), renal carcinoma (Jiang et al, 1998), papillary bladder cancer (Simon et al, 1998), and appear to play a crucial role during aggressive progression of hepatocellular carcinoma (Piao et al, 1998). It is postulated that several, yet unidentified, putative tumour suppressor genes may be located on 4q (Hammoud et al, 1996).…”

Section: Tumour Progression In Prostate Cancer 205mentioning

confidence: 99%

Chromosomal changes during development and progression of prostate adenocarcinomas

Zitzelsberger

Engert²,

Walch

et al. 2001

Br J Cancer

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Summary Chromosomal copy number changes were investigated in 16 prostate carcinomas, 12 prostatic intraepithelial neoplasias (PIN; 4 low-grade and 8 high-grade) adjacent to the invasive tumour areas, and 5 regional lymph node metastases. For this purpose, comparative genomic hybridization (CGH) was performed and a copy number karyotype for each histomorphological entity was created. CGH on microdissected cells from non-neoplastic glands was carried out on 3 different cases to demonstrate the reliability of the overall procedure. None of the non-neoplastic tissue samples revealed chromosome copy number changes. In PIN areas, chromosomal imbalances were detected on chromosomes 7, 8q, Xq (gains), and on 4q, 5q, 8p, 13q and 18q (losses). In the primary tumours, recurrent (at least 25% of cases) gains on chromosomes 12q and 15q, and losses on 2q, 4q, 5q, Xq, 13q and 18q became apparent. Losses on 8p and 6q as well as gains on 8q and of chromosome 7 were also detected at lower frequencies than previously reported. The pooled CGH data from the primary carcinomas revealed a novel region of chromosomal loss on 4q which is also frequently affected in other tumour entities like oesophageal adenocarcinomas and is supposed to harbour a new tumour suppressor gene. Gains on chromosome 9q and of chromosome 16 and loss on chromosome 13q were observed as common aberrations in metastases and primary tumours. These CGH results indicate an accumulation of chromosomal imbalances during the PIN-carcinoma-metastasis sequence and an early origin of tumour-specific aberrations in PIN areas.

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Chromosomal Aberrations Associated With Invasion in Papillary Superficial Bladder Cancer

Cited by 45 publications

References 0 publications

Genetic aberrations of c-myc and CCND1 in the development of invasive bladder cancer

Genetic aberrations of c-myc and CCND1 in the development of invasive bladder cancer

Genetic alterations in urothelial bladder carcinoma

Chromosomal changes during development and progression of prostate adenocarcinomas

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