Assessment of genomic instability in breast cancer and uveal melanoma by random amplified polymorphic DNA analysis

Authors

  • Sarantos Papadopoulos,

    1. Department of Obstetrics and Gynecology, Free University of Berlin, Berlin, Germany
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    • The first 2 authors contributed equally to this work.

  • Thomas Benter,

    Corresponding author
    1. Department of Hematology, Oncology and Tumor Immunology, Robert-Rössle Clinic, Charité, Campus Buch, Humboldt University Berlin, Berlin, Germany
    • Department of Hematology, Oncology and Tumor Immunology, Robert-Rössle Clinic, Charité, Campus Buch, Humboldt University Berlin, Berlin, Germany
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    • The first 2 authors contributed equally to this work.

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  • Gerasimos Anastassiou,

    1. Department of Ophthalmology, Essen University Medical Center, Essen, Germany
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  • Michael Pape,

    1. Division of Internal Medicine, Department of Nephrology, Hanover Medical School, Hanover, Germany
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  • Schaller Gerhard,

    1. Department of Obstetrics and Gynecology, Free University of Berlin, Berlin, Germany
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  • Norbert Bornfeld,

    1. Department of Ophthalmology, Essen University Medical Center, Essen, Germany
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  • Wolf-Dieter Ludwig,

    1. Department of Hematology, Oncology and Tumor Immunology, Robert-Rössle Clinic, Charité, Campus Buch, Humboldt University Berlin, Berlin, Germany
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  • Bernd Dörken

    1. Department of Hematology, Oncology and Tumor Immunology, Robert-Rössle Clinic, Charité, Campus Buch, Humboldt University Berlin, Berlin, Germany
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Abstract

Some types of cancer have been associated with abnormal DNA fingerprinting. We used random amplified polymorphic DNA (RAPD) to generate fingerprints that detect genomic alterations in human breast cancer. Primers were designed by choosing sequences involved in the development of DNA mutations. Seventeen primers in 44 different combinations were used to screen a total of 6 breast cancer DNA/normal DNA pairs and 6 uveal melanoma DNA/normal DNA pairs. Forty-five percent of these combinations reliably detected quantitative differences in the breast cancer pairs, while only 18% of these combinations detected differences in the uveal melanoma pairs. Fourteen (32%) and 12 (27%) primers generated a smear or did not produce any band patterns in the first and second cases, respectively. Taking into account the ability of RAPD to screen the whole genome, our results suggest that the genomic damage in breast cancer is significantly higher than in uveal melanoma. Our study confirms other reports that the molecular karyotypes produced with random priming, called amplotypes, are very useful for assessing genomic damage in cancer. © 2002 Wiley-Liss, Inc.

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