Assessment of Microsatellite Instability in Urine in the Detection of Transitional-Cell Carcinoma of the Bladder

Mourah, S.; Cussenot, O.; Vimont, V.; Desgrandchamps, F.; Teillac, P.; Cochant-Priollet, B.; LeDuc, A.; Fiet, J.; Soliman, H.

doi:10.1097/00005392-199908000-00103

Cited by 17 publications

(29 citation statements)

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“…Steiner et al 53 correctly diagnosed 20 of 21 patients being followed for BC recurrence (n = 11 recurrence; n = 10 no recurrence) using microsatellite analysis with 20 markers in a blinded fashion. Mourah and colleagues 54 reported similar results by detecting microsatellite instability in 10 of 12 patients with BC. While these results are promising, assessment of microsatellite analyses in a larger study, particularly including many subjects without BC, are needed before this technique can be used for clinical diagnosis and early detection efforts.…”

Section: Chromosomementioning

confidence: 66%

Molecular Mechanisms and Pathways in Bladder Cancer Development and Progression

Jung

Messing

2000

Cancer Control

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Background: The basis for bladder cancer development and progression is complex and involves genetic abnormalities. These abnormalities yield phenotypic changes that allow normal transitional cells to becomeity of these new cases, approximately 75%, are limited to the mucosa (stage Ta or Tis) and lamina propria (T1) at presentation, and most of these tumors can be removed by transurethral resection. Recurrence rates are high (30% to 85%), and 10% to 30% of "superficial" tumors (T1 or less) will subsequently progress to muscle invasive disease (stages T2-T4), which has a poorer prognosis. 2 For the remaining 25%, the initial presentation involves muscle invasive disease that will usually relapse with metastases (as well as localized disease persistence) within a median of 2 years if managed only by transurethral resection and intravesical therapy. 3 These data support the heterogeneous nature and malignant potential of transitional cell carcinoma

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Section: Chromosomementioning

confidence: 66%

Molecular Mechanisms and Pathways in Bladder Cancer Development and Progression

Jung

Messing

2000

Cancer Control

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“…MSI has been described in a variety of sporadic cancers, such as colon (Thibodeau et al, 1993), endometrium (Risinger et al, 1993) pancreas and stomach (Han et al, 1993) and prostate (Uchida et al, 1996). Previous studies have also reported a high frequency of MSI in bladder cancer Steiner et al, 1997;Mourah et al, 1998). The finding of MSI in a varying proportion of sporadic cancers suggests that the same type of genetic defects in MMR genes that underlie HNPCC can occur somatically in some sporadic cancers including bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to HNPCC, MSI has been observed in several sporadic tumours (Han et al, 1993; Immunohistochemical analysis of expression and allelotype of mismatch repair genes (hMLH1 and hMSH2) in bladder cancer Chong et al, 1994;Wada et al, 1994;Speicher, 1995). Several studies have reported the occurrence of MSI in bladder cancer (Gonzalez-Zulueta et al, 1993;Mao et al, 1994Mao et al, , 1996Orlow et al, 1994;Uchida et al, 1996;Steiner et al, 1997;Christensen et al, 1998;Mourah et al, 1998). Recently, the tumour spectrum associated with germline mutations of MMR genes in HNPCC cases was found by Aarnio et al (1999) to involve several organs including the uro-epithelium.…”

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confidence: 99%

Immunohistochemical analysis of expression and allelotype of mismatch repair genes (hMLH1 and hMSH2) in bladder cancer

et al. 2001

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Mutation of human homologues of DNA mismatch repair (MMR) genes in tumours has been shown to be associated with the phenomenon of microsatellite instability (MSI). Several studies have reported the occurrence of MSI in bladder cancer, but evidence of involvement of MMR genes in the pathogenesis of this cancer is still unclear. We therefore utilized quantitative immunohistochemical (IHC) image analysis and PCR-based allelotype analysis to determine hMLH1 and hMSH2 genes alteration in a cohort of Egyptian bladder cancer samples. IHC analysis of 24 TCC and 12 SCC revealed marked- intra and intertumour heterogeneity in the levels of expression of the two MMR proteins. One TCC lost MLH1 expression and one lost MSH2, (1/24, 4%), and one SCC lost MSH2 (1/12, 8%). A large proportion of analysed tumours revealed a percentage positivity of less than 50% for MLH1 and MSH2 expression (44% and 69%, respectively). Complete loss of heterozygosity in three dinucleotide repeats lying within, or in close proximity to, hMLH1 and hMSH2 was rare (2/57, (4%) for MLH1 ; and 1/55, (2%) for MSH2 ), however allelic imbalance was detected in 11/57 ( hMLH1 ) and 10/55 ( hMSH2 ) at any of the informative microsatellite loci. These alterations in structure and expression of DNA MMR genes suggest their possible involvement in the tumorigenesis and/or progression of bladder cancer. © 2001 Cancer Research Campaign http://www.bjcancer.com

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“…Therefore, our results with a smaller number of markers but a higher number of investigated samples is comparably high, taking into account that we did not use bladder washings but only spontaneous urine probes for our urine-sediment DNA extraction. Mourah et al 5 demonstrated 83% sensitivity of the method in 31 bladder cancer urine specimens with 100% specificity. Of interest, they also performed the analysis on 6 renal transplanted patients as healthy controls and found the urine probes from these patients to exhibit additional alleles in the MSA owing to the exfoliated donor DNA.…”

Section: Discussionmentioning

confidence: 99%

“…In recent studies MSA was also used to detect tumor-specific DNA alterations in urine sediment samples of patients with TCC of the urinary bladder. 4,5 In a pilot study Steiner et al 4 achieved a sensitivity of 90% for the urinary cancer diagnosis with radiolabeled microsatellite markers. In contrast to cytology, this method is independent of tumor histomorphologic features, and thus offers high sensitivity in well-differentiated tumors.…”

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confidence: 99%

Serum DNA and urine DNA alterations of urinary transitional cell bladder carcinoma detected by fluorescent microsatellite analysis

et al. 2001

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There are no reliable serologic tumor markers for transitional cell carcinoma (TCC) of the urinary bladder and noninvasive urine investigations are inadequate. We used fluorescent microsatellite analysis (MSA) to detect serum DNA and urine-sediment DNA alterations in patients with bladder cancer and prospectively collected fresh tumor, peripheral blood, serum and spontaneous urine specimens from 39 consecutive patients treated for TCC of the bladder to obtain the corresponding DNA. Urinary bladder cancer accounts for approximately 3% of all newly diagnosed malignancies in Western countries. In contrast to most other tumors, bladder carcinoma offers the opportunity of noninvasive diagnosis via urinary cytology. Yet a reliable serologic tumor marker is not available. Follow-up for bladder carcinoma is demanding and time consuming, as most bladder cancers at diagnosis grow superficially and will recur in 70% of cases within 2 years of primary treatment. 1 The intensive follow-up for transitional cell carcinoma (TCC) of the bladder still relies on invasive diagnostic measures such as cystoscopy and bladder washings for urine cytology. Cytology has a low sensitivity in the diagnosis of well-differentiated papillary tumors. A reliable serologic marker and a highly sensitive urinary investigation could reduce the requirement and frequency of invasive procedures during follow-up.In recent studies molecular techniques have proved applicable for the detection of smallest amounts of free circulating tumor DNA in serum and plasma of cancer patients. 2,3 Using microsatellite analysis (MSA) Goessl et al. 3 identified plasma DNA alterations in 63% of patients with renal cell carcinoma. In recent studies MSA was also used to detect tumor-specific DNA alterations in urine sediment samples of patients with TCC of the urinary bladder. 4,5 In a pilot study Steiner et al. 4 achieved a sensitivity of 90% for the urinary cancer diagnosis with radiolabeled microsatellite markers. In contrast to cytology, this method is independent of tumor histomorphologic features, and thus offers high sensitivity in well-differentiated tumors. This molecular genetic assay, not previously looked at in TCC, could reliably identify tumor-specific alterations in the serum of patients and its use in follow-up after radical surgical therapy could lead to early tumor recurrence identification. In the case of superficial bladder cancers, MSA may be helpful in diagnosing local recurrence without the need for invasive measures dependent on morphologic tumor features. We therefore used MSA with 17 highly polymorphic fluorescently labeled microsatellite markers from the chromosomal regions 5q, 8p, 9p, 9q, 13q, 14q, 17p, 17q and 20q to detect serum DNA and sediment-DNA alterations from spontaneous urine samples of 39 consecutive patients treated for TCC of the urinary bladder, to evaluate the sensitivity of the method in the serologic and urinary diagnosis of bladder TCC. MATERIAL AND METHODS Tumor, blood and urine samplingIn 1999, we prospectively collected preo...

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Assessment of Microsatellite Instability in Urine in the Detection of Transitional-Cell Carcinoma of the Bladder

Abstract: Loss of heterozygosity (LOH) and alterations in microsatel-

Cited by 17 publications

References 0 publications

Molecular Mechanisms and Pathways in Bladder Cancer Development and Progression

Molecular Mechanisms and Pathways in Bladder Cancer Development and Progression

Immunohistochemical analysis of expression and allelotype of mismatch repair genes (hMLH1 and hMSH2) in bladder cancer

Serum DNA and urine DNA alterations of urinary transitional cell bladder carcinoma detected by fluorescent microsatellite analysis

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