Molecular Detection of Primary Bladder Cancer by Microsatellite Analysis

Li, Mao; Schoenberg, Mark; Scicchitano, Marshall S.; Erozan, Yener S.; Merlo, Adrian; Schwab, Donna; Sidransky, David

doi:10.1126/science.271.5249.659

Cited by 361 publications

(246 citation statements)

References 22 publications

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“…Furthermore, there is now evidence that in particular tumour types, different microsatellite loci are inherently more likely to show instability than other loci with the same repeat length. Mao et al (1996) have described a method for detection of primary bladder cancers by microsatellite analysis. They screened a series of 60 tri-and tetranucleotide markers against 50 primary bladder cancers.…”

Section: Resultsmentioning

confidence: 99%

Microsatellite instability and loss of heterozygosity in mammary carcinoma and its probable precursors

Dillon

Boer²,

Papadimitriou³

et al. 1997

Br J Cancer

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Summary Microsatellite instability is a form of genetic damage that may be due to defective mismatch repair genes and may be a marker of processes leading to malignancy. We have analysed a series of epithelial hyperplasia of usual type, carcinomas in situ and invasive and metastatic carcinomas from the mammary gland on the assumption that they represent stages in the evolution of mammary carcinoma. Eight markers on chromosomes 3p, 4q, 9p, 11p, 14q, 17p, 17q and Xq were examined for microsatellite instability and loss of heterozygosity. High rates of loss on chromosomes 17p, 17q and Xq indicate that these chromosomal arms contain genes important in mammary carcinogenesis. The rate of microsatellite instability observed in this study was uniformly low, irrespective of the lesion. This implies that microsatellite instability is not a marker of malignancy in most instances of mammary neoplasia.

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Section: Resultsmentioning

confidence: 99%

Microsatellite instability and loss of heterozygosity in mammary carcinoma and its probable precursors

Dillon

Boer²,

Papadimitriou³

et al. 1997

Br J Cancer

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“…All numbering of CAT constructs is relative to the transcription start site for ARF (Mao et al, 1995) and the 5'-most start site for INK4a (Hara et al, 1996). Transfection and CAT assays were performed essentially as described (Robertson and Jones, 1998).…”

Section: Cell Lines Tissue Culture and Drug Treatmentsmentioning

confidence: 99%

“…The unique aspect of the INK4a/ARF locus is that it encodes two distinct cell cycle regulatory proteins, p16INK4a and ARF (alternative reading frame, murine p19ARF, human p14ARF Stott et al, 1998), p16b ) through the use of unique ®rst exons (exon 1a for INK4a and exon 1b for ARF). The exons are driven by unique promoter sequences separated by nearly 20 kilobases (kb) which then splice onto common exon 2 and 3 sequences but utilize di erent reading frames to create two totally unrelated proteins from a shared coding region (Mao et al, 1995;Quelle et al, 1995;Stone et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

“…The role of the p12 transcript could be to produce a protein of as yet unknown function or p12 could be à dummy' transcript acting to reduce the amount of functional INK4a protein, as was originally assigned to the ARF transcript (Mao et al, 1995). Conservation at the DNA and particularly the amino acid level across species is often a useful guide in determining if a transcript has an essential function.…”

Section: Comparison Of Human and Murine Ink4a Intron 1 Dna Sequencesmentioning

confidence: 99%

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Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus

Robertson

Jones

1999

Oncogene

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The INK4a/ARF locus on human chromosome 9p resides at the nexus of two critical cell cycle regulatory pathways, the p53 pathway and the retinoblastoma (pRb) gene pathway. Through the use of shared coding regions and alternative reading frames two distinct proteins are produced: INK4a is a cyclin-dependent kinase inhibitor whereas ARF binds the MDM2 protooncogene and stabilizes p53. We have examined the expression patterns of the INK4a/ARF locus at the RNA level in normal human and murine tissues to determine if these genes are coordinately regulated. We found that both INK4a and ARF were expressed in most tissues at low levels detectable only by RT ± PCR. The pancreas was an exception in that it expressed no detectable ARF mRNA but expressed high levels of INK4a mRNA. Furthermore, human pancreas expressed an additional previously unrecognized splice variant of INK4a, termed p12, through the use of an alternative splice donor site within intron 1. The p12 transcript produced a 12 kD protein composed of INK4a exon 1a and a novel intronderived C-terminus. This novel protein did not interact with cdk4 but was capable of suppressing growth in a pRb-independent manner. The implications of the capacity of the INK4a/ARF locus to encode a third transcript, and for pancreatic cancer, in which the INK4a/ARF locus is nearly always altered, are considered.

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“…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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Molecular Detection of Primary Bladder Cancer by Microsatellite Analysis

Cited by 361 publications

References 22 publications

Microsatellite instability and loss of heterozygosity in mammary carcinoma and its probable precursors

Microsatellite instability and loss of heterozygosity in mammary carcinoma and its probable precursors

Tissue-specific alternative splicing in the human INK4a/ARF cell cycle regulatory locus

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

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