Open AccessMolecular Cytogenetic Analysis of 17 Renal Cancer Cell Lines: Increased Copy Number at 5q31‐33 in Cell Lines from Nonpapillary Carcinomas
Author(s) -
Yang ZengQuan,
Yoshida Mitsuaki A.,
Fukuda Yoji,
Kurihara Naoki,
Nakamura Yusuke,
Inazawa Johji
Publication year - 2000
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.2000.tb00927.x
Subject(s) - comparative genomic hybridization , fluorescence in situ hybridization , cytogenetics , biology , papillary renal cell carcinomas , cancer research , pathology , renal cell carcinoma , renal pelvis , chromosome 7 (human) , cell culture , carcinoma , chromosome , microbiology and biotechnology , kidney , genetics , gene , medicine
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.