Molecular Cytogenetic Analysis of 17 Renal Cancer Cell Lines: Increased Copy Number at 5q31-33 in Cell Lines from Nonpapillary Carcinomas |
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Authors: | Zeng-Quan Yang Mitsuaki A Yoshida Yoji Fukuda Naoki Kurihara Yusuke Nakamura Johji Inazawa |
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Institution: | Department of Molecular Cytogenetics, Division of Genetics, Medical Research Institute, Tokyo Medical and Dental University, 1–5–45 Yushima, Bunkyo-ku, Tokyo 113–8510;Laboratory of Molecular Medicine, Institute of Medical Science, University of Tokyo, 4–6–1 Shirokanedai, Minato-ku, Tokyo 108–8639 |
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Abstract: | Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in cell lines derived from 13 nonpapillary renal-cell carcinomas (RCCs), two papillary RCCs, one renal squamous-cell carcinoma, and one transitional-cell carcinoma of the renal pelvis. Aberrations were found in all 17 lines. The most frequent changes in nonpapillary RCC cell lines were gains of 5q (85%), 7q (69%), 8q (69%) and 1q (54%) and losses of 3p (92%), 8p (77%), 4q (62%) and 14q (54%). High-level gains (HLGs) were detected at 4q12, 5p, 5q23-33, 7q22-qter, 8q23-24, 10q21-qter, 12p and 12q13-22. By means of fluorescence in situ hybridization (FISH) we narrowed the smallest common region involving 5q gains to the genomic segment between D5S642 and D5S673, and found that the HLG at 4q12 possibly involved amplifications of c-kit and PDGFRA . Two papillary RCC cell lines showed gains of entire chromosomes 7, 12 and 17. The CGH data reported here should help to facilitate the choice of individual renal-tumor cell lines for exploring target genes in regions of interest. |
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Keywords: | Renal cell carcinoma (RCC) CGH FISH Gene amplification |
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