Molecular cytogenetic analysis of 11 new breast cancer cell lines

Abstract

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%), 3q (45%) and 7p (45%), whereas losses were most frequent at Xp (54%), 8p (45%), 18q (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. © 1999 Cancer Research Campaign

Trastuzumab signaling in ErbB2-overexpressing inflammatory breast cancer correlates with X-linked inhibitor of apoptosis protein expression

“…A distinct mechanism of increased expression of XIAP and survivin, key members of the BIRC/IAP protein family post-trastuzumab treatment, was observed in ErbB2-overexpressing SUM190PT IBC cells, an established ErbB2-overexpressing IBC line isolated from a primary tumor of an IBC patient (30). In contrast, decrease in tumor cell viability in response to treatment with the small-molecule ErbB2-targeting agent, GW583340, correlated with a significant decrease in XIAP and survivin abundance.…”

“…DMEM was purchased from Mediatech. Insulin, hydrocortisone, HEPES, penicillin, streptomycin, ethanolamine, transferrin, sodium selenite, and epidermal growth factor were all purchased from Sigma Chemical Co. All SUM lines were cultured as per the manufacturer's instructions and as described previously (30). SKBR3 cells were routinely cultured in modified McCoy's 5a medium with 1.5 mmol/L L-glutamine adjusted to contain 2.2 g/L sodium bicarbonate and 10% fetal bovine serum.…”

E-cadherin transcriptional downregulation by promoter methylation but not mutation is related to epithelial-to-mesenchymal transition in breast cancer cell lines

“…MPE600 and SK-BR-5 were provided by Dr F Waldman (California Pacific Medical Centre, San Francisco, CA, USA) and Dr E Stockert (Sloan-Kettering Institute for Cancer Research, New York, NY, USA), respectively. Dr SP Ethier donated SUM44PE (Ethier et al, 1993) and SUM185PE (Forozan et al, 1999). OCUB-F was obtained from the Riken Gene Bank.…”

Absence of major defects in non-homologous DNA end joining in human breast cancer cell lines

“…Two major arguments suggest that breast cancer cells might be deficient in DNA double-strand break (DSB) repair. First, FISH, standard karyotype and more recently multicolour analysis of breast cancer cells have revealed a very high frequency of chromosome rearrangements (Davidson et al, 2000;Forozan et al, 2000;Kytola et al, 2000;Loveday et al, 2000). Second, recent advances in the study of the functions of BRCA1 and BRCA2 tumour suppressor genes indicate that their products play important roles in DSB repair and chromosome stability (Khanna and Jackson, 2001;Patel et al, 1998;Shen et al, 1998;Moynahan et al, 1999Moynahan et al, , 2001Snouwaert et al, 1999;Yu et al, 2000).…”