Aneusomy of chromosomes 7 and 17 predicts the recurrence of transitional cell carcinoma of the urinary bladder

Watters, A.D.; Ballantyne, Stuart; Going, James J.; Grigor, Ken; Bartlett, John M.S.

doi:10.1046/j.1464-410x.2000.00326.x

Cited by 38 publications

(52 citation statements)

References 18 publications

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“…Furthermore, it is of interest to note that the rate of genetic abnormalities is similar when comparing the data from patients who progress from nonmuscle-invasion and those who present with muscle invasion. In this study, and previously, we have shown that there are higher rates of aneusomy in patients who progress to muscle invasion compared to those who recur with pTa/pT1 disease (Watters et al, 2000(Watters et al, , 2002. Muscle-invasive TCCs are characterised by a large number of cytogenetic alterations including overrepresentation of 8q and 11q13 (Tomovska et al, 2001).…”

Section: Discussionsupporting

confidence: 65%

“…The tissue sections were assessed for extent of digestion as previously outlined (Watters et al, 2000). Tissue sections were denatured in 70% formamide, 26SSC pH 7 -8 at 728C for 5 min on the Omnislide hybridisation module (Hybaid, UK Ltd), dehydrated and air-dried.…”

Section: Fluorescence In Situ Hybridisation (Fish)mentioning

confidence: 99%

“…Control sections from normal bladder tissue obtained from post mortem normal bladder were included in the analysis. Values for disomy were derived from the analysis of these tissue sections as previously reported (Bartlett et al, 1998;Watters et al, 2000).…”

Section: Scoring Criteriamentioning

confidence: 99%

“…Previous research within this laboratory demonstrated that polysomy of chromosomes 9, 7 and 17 are associated with recurrence (Bartlett et al, 1998, Watters et al, 2000, but that these genetic events are not linked with polyploidy (Bartlett et al, 1999). A small study within this laboratory investigating the drug metabolising enzyme NAT2 (the gene is located at chromosome 8p22) in TCC recurrence or progression suggested that polysomy 8 was associated with disease progression .…”

mentioning

confidence: 95%

“…Following on from previous studies within this laboratory (Bartlett et al, 1998(Bartlett et al, , 1999Watters et al, 2000Watters et al, , 2001) which associated specific chromosomal aberrations with recurrence or progression, we hypothesised that alteration of key cell cycle modulators c-myc and CCND1 via gene alterations drives progression of superficial and locally invasive TCC (pTa/pT1). This study determined chromosome and gene copy number by FISH in a cohort of patients with either detrusor muscle invasive TCC at presentation or who developed detrusor muscle invasive TCC following a presentation with non-muscle invasive (pTa/pT1) TCC.…”

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confidence: 99%

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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: Discussionsupporting

confidence: 65%

Section: Fluorescence In Situ Hybridisation (Fish)mentioning

confidence: 99%

Section: Scoring Criteriamentioning

confidence: 99%

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confidence: 95%

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confidence: 99%

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

et al. 2002

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Identification of loci associated with putative recurrence genes in transitional cell carcinoma of the urinary bladder

Edwards

Duncan

Going

et al. 2002

The Journal of Pathology

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Following an earlier study linking monosomy 9 with recurrence of transitional cell carcinomas (TCCs) of the urinary bladder, 109 primary and recurrent TCCs (from 47 patients) were examined to explore genetic alterations at chromosome 9 associated with recurrence. Patient DNA was microdissected and extracted from archival tissue sections and analysed for loss of heterozygosity (LOH) at three regions on chromosome 9 where tumour suppressor genes (TSGs) are known to reside (INK 4A, DBC1, and TSC1). Patients were categorized into two groups, non-recurrent TCC (NR, n=18) and recurrent TCC (REC, n=29). It was noted that 12% of NR tumours, compared with 54% of REC primary tumours (p=0.01), had LOH at all informative markers spanning the TSC1 region. The risk of recurrence was significantly higher in patients with deleted TSC1 than in those who retained the TSC1 region (p=0.035). Levels of LOH at DBC1 or INK 4A were not significantly different in NR tumours than in REC primary tumours and recurrence-free survival was not affected by loss of either of these genes. Loss of all informative markers spanning chromosome 9 was observed in 0% of NR tumours compared with 25% of REC primary tumours (p=0.04). The probability of recurrence was also significantly increased in patients who had LOH at all informative markers spanning chromosome 9 (p=0.016), confirming earlier fluorescence in situ hybridization results. This study provides further evidence that recurrence in bladder cancer is a distinct event, with underlying molecular causes. It also identifies the TSC1 locus as a candidate for a TSG, which drives recurrence in a proportion of TCC patients. Loss of all informative markers, including those residing in the TSC1 region, spanning chromosome 9 was also linked to recurrence.

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The clinical evaluation of HER‐2 status: which test to use?

Bartlett

Mallon

Cooke

2003

The Journal of Pathology

122

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Accurate determination of the status of the type I receptor tyrosine kinase HER-2 in breast carcinomas provides significant insight into patient prognosis and may also inform selection of chemotherapeutic and hormonal treatments. At present, however, the single most important application of HER-2 testing is in the selection of patients for treatment with targeted therapies such as Herceptin. Although, based on current literature, fluorescence in situ hybridization (FISH) detection of HER-2 gene amplification may provide more accurate information in this context, this method is not yet widely available. Therefore, screening by immunohistochemistry (IHC) for HER-2 protein, backed by rigorous quality controls and FISH testing of equivocal cases with intermediate staining intensity, remains the current practice. In laboratories with highly standardized testing and quality assurance procedures, this protocol appears highly effective. Improvements in fixation procedures, standardization of antibodies, and use of automated image analysis may all increase the precision of IHC testing. However, on the basis of current data, there is a case to be made for the wider implementation of FISH testing to determine HER-2 status in breast cancer.

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Aneusomy of chromosomes 7 and 17 predicts the recurrence of transitional cell carcinoma of the urinary bladder

Cited by 38 publications

References 18 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

Identification of loci associated with putative recurrence genes in transitional cell carcinoma of the urinary bladder

The clinical evaluation of HER‐2 status: which test to use?

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