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nature portfolio privacy policy nature med 4 nature advertising 0/ reprints breast cancer development high-throughput molecular profiling c-erbb-2 gene amplification social media selective media sum-159pt cells personal data human breast cancer molecular cytogenetics breast cancer cells breast carcinoma cells molecular cytogenetic analysis primary breast cancer data protection cancer development human breast cancers permissions breast cancer based drosophila aurora kinase functional analysis human colorectal cancers dna sequence amplification privacy localized dna amplifications chromosomal gains cancer biology cell lines explore content similar content epidermal growth factor hormone receptor positive comparative genomic hybridization amplified dna sequences journals search log high-level myc tyrosine phosphorylated erbb-2 european economic area metstatic lymph node progressively elevated levels michigan medical school predicts poor outcome comparative transcriptional analyses amplification-related gain breast cancer

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         headline:Molecular cytogenetic analysis of 11 new breast cancer cell lines
         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.
         datePublished:1999-11-26T00:00:00Z
         dateModified:2011-11-16T00:00:00Z
         pageStart:1328
         pageEnd:1334
         sameAs:https://doi.org/10.1038/sj.bjc.6695007
         keywords:
            molecular cytogenetics
            FISH
            CGH
            chromosomal aberrations
            oncogene amplification
            Biomedicine
            general
            Cancer Research
            Epidemiology
            Molecular Medicine
            Oncology
            Drug Resistance
         image:
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               1532-1827
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            name:Nature Publishing Group UK
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      headline:Molecular cytogenetic analysis of 11 new breast cancer cell lines
      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.
      datePublished:1999-11-26T00:00:00Z
      dateModified:2011-11-16T00:00:00Z
      pageStart:1328
      pageEnd:1334
      sameAs:https://doi.org/10.1038/sj.bjc.6695007
      keywords:
         molecular cytogenetics
         FISH
         CGH
         chromosomal aberrations
         oncogene amplification
         Biomedicine
         general
         Cancer Research
         Epidemiology
         Molecular Medicine
         Oncology
         Drug Resistance
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            1532-1827
            0007-0920
         volumeNumber:81
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         name:Nature Publishing Group UK
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                  address:
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      name:Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, USA
      name:Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, USA
      name:Department of Radiation Oncology, Division of Radiation and Cancer Biology, University of Michigan Medical School, 7312 Cancer Center, 1500 E. Medical Center Dr, Ann Arbor, USA

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