Molecular cytogenetic analysis of 11 new breast cancer cell lines

被引:159
作者
Forozan, F
Veldman, R
Ammerman, CA
Parsa, NZ
Kallioniemi, A
Kallioniemi, OP
Ethier, SP
机构
[1] Univ Michigan, Sch Med, Dept Radiat Oncol, Div Radiat & Canc Biol,Canc Ctr 7312, Ann Arbor, MI 48109 USA
[2] Natl Human Genome Res Inst, Canc Genet Branch, NIH, Bethesda, MD 20892 USA
关键词
molecular cytogenetics; FISH; CGH; chromosomal aberrations; oncogene amplification;
D O I
10.1038/sj.bjc.6695007
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We describe a survey of genetic changes by comparative genomic hybridization (CGH) in 11 human breast cancer cell lines recently established in our laboratory. The most common gains took place at 8q (73%), 1q (64%), 7q (64%), 39 (45%) and 79 (45%), whereas losses were most frequent at Xp (54%), 8p (45%), 189 (45%) and Xq (45%). Many of the cell lines displayed prominent, localized DNA amplifications by CGH. One-third of these loci affected breast cancer oncogenes, whose amplifications were validated with specific probes: 17q12 (two cell lines with ERBB2 amplifications), 11q13 (two with cyclin-D1), 8p11-p12 (two with FGFR1) and 10q25 (one with FGFR2). Gains and amplifications affecting 8q were the most common genetic alterations in these cell lines with the minimal, common region of involvement at 8q22-q23. No high-level MYC (at 8q24) amplifications were found in any of the cell lines. Two-thirds of the amplification sites took place at loci not associated with established oncogenes, such as 1q41-q43, 7q21-q22, 7q31, 8q23, 9p21-p23, 11p12-p14, 15q12-q14, 16q13-q21, 17q23, 20p11-p12 and 20q13. Several of these locations have not been previously reported and may harbour important genes whose amplification is selected for during cancer development. In summary, this set of breast cancer cell lines displaying prominent DNA amplifications should facilitate discovery and functional analysis of genes and signal transduction pathways contributing to breast cancer development. (C) 1999 Cancer Research Campaign.
引用
收藏
页码:1328 / 1334
页数:7
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