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Molecular cytogenetic analysis of 11 new breast cancer cell lines

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 (...

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Autores principales: Forozan, F, Veldman, R, Ammerman, C A, Parsa, N Z, Kallioniemi, A, Kallioniemi, O-P, Ethier, S P
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1999
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362964/
https://www.ncbi.nlm.nih.gov/pubmed/10604729
http://dx.doi.org/10.1038/sj.bjc.6695007
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author Forozan, F
Veldman, R
Ammerman, C A
Parsa, N Z
Kallioniemi, A
Kallioniemi, O-P
Ethier, S P
author_facet Forozan, F
Veldman, R
Ammerman, C A
Parsa, N Z
Kallioniemi, A
Kallioniemi, O-P
Ethier, S P
author_sort Forozan, F
collection PubMed
description 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
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spelling pubmed-23629642009-09-10 Molecular cytogenetic analysis of 11 new breast cancer cell lines Forozan, F Veldman, R Ammerman, C A Parsa, N Z Kallioniemi, A Kallioniemi, O-P Ethier, S P Br J Cancer Regular Article 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 Nature Publishing Group 1999-12 /pmc/articles/PMC2362964/ /pubmed/10604729 http://dx.doi.org/10.1038/sj.bjc.6695007 Text en Copyright © 1999 Cancer Research Campaign https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Regular Article
Forozan, F
Veldman, R
Ammerman, C A
Parsa, N Z
Kallioniemi, A
Kallioniemi, O-P
Ethier, S P
Molecular cytogenetic analysis of 11 new breast cancer cell lines
title Molecular cytogenetic analysis of 11 new breast cancer cell lines
title_full Molecular cytogenetic analysis of 11 new breast cancer cell lines
title_fullStr Molecular cytogenetic analysis of 11 new breast cancer cell lines
title_full_unstemmed Molecular cytogenetic analysis of 11 new breast cancer cell lines
title_short Molecular cytogenetic analysis of 11 new breast cancer cell lines
title_sort molecular cytogenetic analysis of 11 new breast cancer cell lines
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362964/
https://www.ncbi.nlm.nih.gov/pubmed/10604729
http://dx.doi.org/10.1038/sj.bjc.6695007
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