ArticleThe American journal of pathology1995
Detection of chromosomal imbalances in transitional cell carcinoma of the bladder by comparative genomic hybridization.
Article in The American journal of pathology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 114 citations in OpenAlex.
- Fluorescence in situ hybridization as prognostic predictor of tumor recurrence during treatment with Bacillus Calmette-Guérin therapy for intermediate- and high-risk non-muscle-invasive bladder cancer.Medical oncology (Northwood, London, England) · 2017Trial
- Clinical impact of copy number variation changes in bladder cancer samples.Experimental and therapeutic medicine · 2021Article
- Novel role of BRCA1 interacting C-terminal helicase 1 (BRIP1) in breast tumour cell invasion.Journal of cellular and molecular medicine · 2020Article
- Molecular biology of bladder cancer.Hematology/oncology clinics of North America · 2015Review
- Mapping of the chromosomal amplification 1p21-22 in bladder cancer.BMC research notes · 2014Article
- Identification of prefoldin amplification (1q23.3-q24.1) in bladder cancer using comparative genomic hybridization (CGH) arrays of urinary DNA.Journal of translational medicine · 2013Article
- Article
- Chromosomal changes in uroepithelial carcinomas.Cell & chromosome · 2005Article
- Effects of transforming growth interacting factor on biological behaviors of gastric carcinoma cells.World journal of gastroenterology · 2005Article
- Advanced molecular cytogenetics in human and mouse.Expert review of molecular diagnostics · 2004Review
- Article
- High-resolution analysis of genomic copy number alterations in bladder cancer by microarray-based comparative genomic hybridization.Oncogene · 2004Article
- Loss of p63 expression is associated with tumor progression in bladder cancer.The American journal of pathology · 2002Article
- High-throughput copy number analysis of 17q23 in 3520 tissue specimens by fluorescence in situ hybridization to tissue microarrays.The American journal of pathology · 2002Article
- Amplification pattern of 12q13-q15 genes (MDM2, CDK4, GLI) in urinary bladder cancer.Oncogene · 2002Article
- Functional analysis of the mismatch repair system in bladder cancer.British journal of cancer · 2001Article
- Tumour-amplified kinase BTAK is amplified and overexpressed in gastric cancers with possible involvement in aneuploid formation.British journal of cancer · 2001Article
- High-throughput tissue microarray analysis of cyclin E gene amplification and overexpression in urinary bladder cancer.The American journal of pathology · 2000Article
- DNA copy number changes in Schistosoma-associated and non-Schistosoma-associated bladder cancer.The American journal of pathology · 2000Article
- Loss of FHIT expression in transitional cell carcinoma of the urinary bladder.The American journal of pathology · 2000Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Comparative genomic hybridization (CGH) was applied for a comprehensive screening of chromosomal aberrations in 14 transitional cell carcinomas of the bladder of different grade and stage. The results were compared in a number of selected cases with those obtained by restriction fragment length polymorphism analyses and targeted fluorescence in situ hybridization. Distinct amplifications, found with CGH, were located on 3p22-24, 10p13-14, 12q13-15, 17q22-23, 18p11, and 22q11-13. These high copy number amplifications and the frequency of imbalances involving chromosome 5, occurring in 4 of 14 cases, have not yet been identified in transitional cell carcinomas. Apart from these new aberrations, imbalances were detected in 3 or more cases for chromosomes 9 and 11, as already described previously in the literature. In four tumors, the copy number of specific chromosomal regions was also analyzed by interphase cytogenetics. Although in most instances the CGH data were confirmed, in one tumor, distinct differences were observed, possibly a result of heterogeneity of the tumor cell population. Furthermore, the CGH data were compared with loss of heterozygosity as revealed by restriction fragment length polymorphism analysis in the same tumors. In 80% of informative cases, no loss was detected by restriction fragment length polymorphism or by CGH. Of the 15 cases of loss of heterozygosity, 7 showed a loss also with CGH, whereas in 8 cases no loss was observed. In summary, CGH is a fast method to obtain a comprehensive picture of chromosomal imbalances in transitional cell carcinomas, including a number of previously unknown genomic alterations such as high level amplifications.
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7778674PMC1870895W1581910748What OpenQuestion holds
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