Characterization of chromosome 9 deletions in transitional cell carcinoma by microsatellite assay

Aj, Linnenbach; Lb, Pressler; Ba, Seng; Bs, Kimmel; Je, Tomaszewski; Sb, Malkowicz

doi:10.1093/hmg/2.9.1407

Cited by 59 publications

(28 citation statements)

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“…Loss of heterozygosity in chromosome 9q has been found in approximately 70% of superficial bladder tumors. Meanwhile, a deletion at the long arm of chromosome 9 between 9q12 and 9q34 was also observed in invasive transitional-cell carcinomas [24][25][26]. These observations suggest inactivation of a suppressor gene in this region, occurring in early-stage as well as advanced urothelial neoplasm.…”

Section: Discussionmentioning

confidence: 99%

Downregulated gelsolin expression in hyperplastic and neoplastic lesions of the prostate

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Downregulated gelsolin expression in hyperplastic and neoplastic lesions of the prostate

et al. 1999

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“…Recently, interest has centred on loss on chromosome 9p2l in TCC. The identification of a tumoursuppresser gene (MTS 1,p16) at this locus and the high frequency of its loss in TCC (Linnenbach et al, 1993;Devlin et al, 1994;Keen and Knowles, 1994) confirm the importance of 9p2l as the site of an early bladder cancer event. Between 28% and 60% of tumours have been shown to lack copies of all chromosome 9 loci (Keen and Knowles, 1994;Orlow et al, 1994;Habuchi et al, 1995;Sauter et al, 1995) tested.…”

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confidence: 91%

Is chromosome 9 loss a marker of disease recurrence in transitional cell carcinoma of the urinary bladder?

Bartlett

Watters²,

Ballantyne³

et al. 1998

Br J Cancer

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Summary Investigation of transitional cell carcinoma of the urinary bladder (TCC) patients classified by recurrence and/or progression has demonstrated that loss of chromosome 9, as detected by FISH analysis of the pericentromeric classical satellite marker at 9q12, occurs early. A total of 105 TCCs from 53 patients were analysed in situ by two independent observers for loss of chromosome 9 using quantitative fluorescence in situ hybridization (FISH). All 53 primary tumours were evaluated for chromosomes 9, 7 and 17. Normal ranges for chromosomal copy number were defined for normal skin epidermis and bladder epithelium. Values for chromosome 9 copy number outwith the range 1.51-2.10 (mean ± 3 x s.d. of normal values) were significantly abnormal. Twenty-five TCCs were detected with consistent monosomic scores. Of 89 TCCs, in which multiple tumour areas were analysed, 85 tumours (96%) demonstrated the same chromosome 9 copy number in all areas (2-6) analysed; only three tumours demonstrated heterogeneity for this locus. A total of 36% (12 out of 33) of patients with subsequent disease recurrence demonstrated loss of chromosome 9 in their primary and all subsequent TCCs analysed. Only a single patient (n = 20) with non-recurrent TCC showed loss of chromosome 9 (P = 0.0085). Of 53 primary tumours, eight showed significant elevation of chromosome 17. Of these patients, six demonstrated elevation in chromosome 7 copy number. No abnormalities were observed in non-recurrent patients. This study describes rapid quantitation of chromosomal copy number by FISH using a pericentromeric probe for chromosome 9 in TCC of the urinary bladder. Routinely fixed and processed material was evaluated without disaggregation. Strict quality control of FISH demonstrated that this technique was reproducible in a clinical environment and could be used to detect genetic changes relevant to patient outcome. It is proposed that loss of chromosome 9 from primary TCC of the urinary bladder identified patients at high risk of recurrence and possible progression.

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“…Microsatellite repeats were amplified by polymerase chain reaction (PCR) performed as described. 42,43 The 100-µL reaction volume contained 50 ng of genomic DNA template, 0.4 µmol/L of each oligonucleotide primer, 200 µmol/L each of deoxycytidine triphosphate (dCTP), deoxyadenosine triphosphate (dATP), deoxythymidine triphosphate (dTTP), 2.5 µmol/L of were electrophoresed on denaturing 7 mol/L urea/6% polyacrylamide gels, vacuum-dried, and exposed to preflashed X-ray Kodak film.…”

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confidence: 99%

Multiple Genetic Alterations, 4Q28, A New Suppressor Region, and Potential Gender Differences in Human Hepatocellular Carcinoma

Hammond¹,

Jeffers²,

Carr³

et al. 1999

Hepatology

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Primary hepatocellular carcinomas (HCCs) of different etiologies were studied to determine the rate of alteration of several genetic regions previously associated with the HCC phenotype. The focus of our study was to identify the frequency of genetic alterations within individual HCCs and their distribution among male and female cases. Genetic differences were evaluated between DNA isolated from tumor (T) and corresponding non-tumor (N) tissue using short tandem repeat (STR)-microsatellites and restriction fragment length polymorphism (RFLP) analyses. Twenty-eight HCC cases were studied with polymorphic markers from different parts of the genome. Three or more loci were identified with genetic alterations from 28 loci tested in 63% of HCC cases. Human hepatocellular carcinoma (HCC) remains a leading cause of cancer death worldwide. HCC has a very poor prognosis, and there is only limited understanding of the molecular events that lead to uncontrolled proliferation of the liver parenchymal cells. Several etiologic factors have been identified as high risk factors in association with HCC development, including previous infection with hepatitis B virus (HBV), hepatitis C virus (HCV), exposure to aflatoxin, and alcohol-induced cirrhosis. 1-4 However, it remains unclear how these agents affect hepatocyte growth, the transformation process, or both.Current research has focused on identifying the genetic region(s) in which a mutation leads to transformation in the hepatocyte and malignant proliferation in the liver because neoplasia is thought to result from the initiation and accumulation of genetic mutations in a multistep process. Genetic evolution of the tumor phenotype is best defined in colorectal cancer in which several sequential mutations have been identified in association with the stage of the disease. 5,6 Alterations of several chromosomal regions have been identified in HCC. 7-38 Some data suggest that certain HCC causes are associated with specific genetic alterations. 25,26,36 p53 is the only gene in which specific mutations have been associated with HCC, but even these mutations are recognized as later alterations in HCC development. [26][27][28][29] Epidemiological studies document the higher incidence of HCC among men than women but so far no correlation with genetic data was implicated. A recent study in 120 HCCs documented frequent loss of heterozygosity (LOH) in chromosome regions 1p, 1q, 2q, 4q, 6q, 8p, 9q, 16p, 16q, and 17p. 34 Despite a long list of loci with frequent LOH in HCCs the sequence of these mutations in HCC development is not understood.We and others have identified a high incidence of genetic alteration in the short arm of chromosome 1 in HCCs of different causes. [30][31][32][33] We now report that the majority of our HCC cases have multiple genetic alterations. The most frequent target for genetic change in HCCs analyzed is the 1p36 region. The frequent LOH in 1p36.1, 1p36.3, 4q28, 13q14, and 17p13 indicates important HCC suppressors in the vicinity of these regions. The 4q28 locus...

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Characterization of chromosome 9 deletions in transitional cell carcinoma by microsatellite assay

Cited by 59 publications

References 0 publications

Downregulated gelsolin expression in hyperplastic and neoplastic lesions of the prostate

Downregulated gelsolin expression in hyperplastic and neoplastic lesions of the prostate

Is chromosome 9 loss a marker of disease recurrence in transitional cell carcinoma of the urinary bladder?

Multiple Genetic Alterations, 4Q28, A New Suppressor Region, and Potential Gender Differences in Human Hepatocellular Carcinoma

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