We describe a survey of genetic changes by comparative genomic hybridizatio
n (CGH) in 11 human breast cancer cell lines recently established in our la
boratory. 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, l
ocalized 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 amplif
ications affecting 8q were the most common genetic alterations in these cel
l 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. Tw
o-thirds of the amplification sites took place at loci not associated with
established oncogenes, such as 1q41-q43, 7q21-q22, 7q31, 8q23, 9p21-p23, 11
p12-p14, 15q12-q14, 16q13-q21, 17q23, 20p11-p12 and 20q13. Several of these
locations have not been previously reported and may harbour important gene
s whose amplification is selected for during cancer development. In summary
, this set of breast cancer cell lines displaying prominent DNA amplificati
ons should facilitate discovery and functional analysis of genes and signal
transduction pathways contributing to breast cancer development. (C) 1999
Cancer Research Campaign.