Comparative genomic hybridization analysis of transitional cell carcinomas of the renal pelvis

Rigola, M A; Fuster, Carme; Casadevall, Carme; Bernués, Marta; Caballı́n, Marı́a Rosa; Gelabert, Antoni; Egozcue, J.; Miró, Rosa

doi:10.1016/s0165-4608(00)00426-x

Cited by 23 publications

(16 citation statements)

References 14 publications

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“…10 In addition, Bruch et al 11 reported 6p22 gains in 6 of 8 bladder cancer cell lines. Recently, Veltman et al 12 confirmed the metaphase CGH findings using array-based CGH to show copy number gains at 6p22 in 11 of a series of 41 bladder tumors.…”

mentioning

confidence: 99%

Defining a 0.5-Mb Region of Genomic Gain on Chromosome 6p22 in Bladder Cancer by Quantitative-Multiplex Polymerase Chain Reaction

Evans

Gallie

Jewett

et al. 2004

The American Journal of Pathology

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Urothelial carcinomas, or transitional cell carcinomas, represent the vast majority of human bladder cancers. Early molecular events associated with superficial bladder cancers include losses on chromosome 9p/9q and mutations in the p53 and retinoblastoma tumor suppressor genes. 1,2 The genomic alterations associated with disease progression, defined as the evolution of superficial bladder tumors to higher pathological stages, are complex and poorly understood. Conventional metaphase-based comparative genomic hybridization (CGH) has been used by several groups of investigators to study copy number imbalances in bladder cancer specimens of all stages and grades. These studies have illustrated the genomic complexity of bladder cancer and have identified recurrent regions of DNA copy number increase or high level amplification on several chromosomes including; 1q, 5p, 6p, 8q, 10p, 12q, 17q, and 20q. 3-9 These genomic regions are thought to contain oncogenes that may be important in tumor progression.Metaphase CGH studies have demonstrated copy number gains or high level amplifications at 6p22 in 7 to 55% of urothelial carcinomas, involving primarily the bladder, 3-9 but also those arising in the renal pelvis. 10 In addition, Bruch et al 11 reported 6p22 gains in 6 of 8 bladder cancer cell lines. Recently, Veltman et al 12 confirmed the metaphase CGH findings using array-based CGH to show copy number gains at 6p22 in 11 of a series of 41 bladder tumors. The changes at 6p22 in bladder cancer have been associated with high tumor cell proliferative activity, 9 tumors of high histological grade that are predominantly invasive, 3-9 and patients with distant metastases at initial presentation. 8 Based on these findings,

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confidence: 99%

Defining a 0.5-Mb Region of Genomic Gain on Chromosome 6p22 in Bladder Cancer by Quantitative-Multiplex Polymerase Chain Reaction

Evans

Gallie

Jewett

et al. 2004

The American Journal of Pathology

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“…Comparative genomic hybridization (CGH) analysis was performed as described previously [28]. DNA for tests (hASCs and FP-ASCs) was labeled with Spectrum Red-dUTP, whereas reference DNA was labeled with Spectrum GreendUTP by nick translation using a commercial kit (Vysis).…”

Section: Determination Of Cell Senescencementioning

confidence: 99%

Fast-Proliferating Adipose Tissue Mesenchymal-Stromal-Like Cells for Therapy

Aguilar

Bagó²,

Soler‐Botija³

et al. 2014

Stem Cells and Development

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Human mesenchymal stromal cells, whether from the bone marrow or adipose tissue (hASCs), are promising cell therapy agents. However, generation of abundant cells for therapy remains to be a challenge, due to the need of lengthy expansion and the risk of accumulating genomic defects during the process. We show that hASCs can be easily induced to a reversible fast-proliferating phenotype (FP-ASCs) that allows rapid generation of a clinically useful quantity of cells in < 2 weeks of culture. Expanded FP-ASCs retain their finite expansion capacity and pluripotent properties. Despite the high proliferation rate, FP-ASCs show genomic stability by array-comparative genomic hybridization, and did not generate tumors when implanted for a long time in an SCID mouse model. Comparative analysis of gene expression patterns revealed a set of genes that can be used to characterize FP-ASCs and distinguish them from hASCs. As potential candidate therapeutic agents, FP-ASCs displayed high vasculogenic capacity in Matrigel assays. Moreover, application of hASCs and FP-ASCs in a fibrin scaffold over a myocardium infarct model in SCID mice showed that both cell types can differentiate to endothelial and myocardium lineages, although FP-ASCs were more potent angiogenesis inducers than hASCs, at promoting myocardium revascularization.

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“…Un caryotype anormal a été décrit dans 64 à 80 % des cas de TVES [56][57][58]. Les premiers caryotypes réalisés ont mis en évidence la trisomie du chromosome 7 (30 %) et la perte du chromosome Y (25 % à 50 %), comme étant les deux altéra-tions les plus fréquentes [56,57].…”

Section: Instabilité Chromosomiqueunclassified

“…Les pertes sont dans les régions chromosomiques suivantes : 2q, 8p, 11p, 13q, 14q, 17p, 18q et Xq [58]. Des gains ou amplifications ont été décrits sur les sites chromosomiques suivants : 8q (40 %), 1q (30 %), 2p (30 %), 3p, 3q, 6p, 9p, 11q, 12q, 17q et l'intégralité du chromosome 20 (30 %) [58]. Des altérations similaires ont été observées dans les TVES et les tumeurs de la vessie notamment pour les pertes en 2q, 8p, 9q, 11p, 13q, 17p, 18q et les gains en 1q, 6p, 8q et 17q [58] mais leur fréquence était plus élevée s'agissant des TVES [12].…”

Section: Instabilité Chromosomiqueunclassified

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Voies de carcinogenèse et histoire naturelle des tumeurs de la voie excrétrice supérieure : état de l’art pour le rapport annuel de l’Association française d’urologie

Seisen

Cancel‐Tassin

Colin

et al. 2014

Progrès en Urologie

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Comparative genomic hybridization analysis of transitional cell carcinomas of the renal pelvis

Cited by 23 publications

References 14 publications

Defining a 0.5-Mb Region of Genomic Gain on Chromosome 6p22 in Bladder Cancer by Quantitative-Multiplex Polymerase Chain Reaction

Defining a 0.5-Mb Region of Genomic Gain on Chromosome 6p22 in Bladder Cancer by Quantitative-Multiplex Polymerase Chain Reaction

Fast-Proliferating Adipose Tissue Mesenchymal-Stromal-Like Cells for Therapy

Voies de carcinogenèse et histoire naturelle des tumeurs de la voie excrétrice supérieure : état de l’art pour le rapport annuel de l’Association française d’urologie

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