Disruption of the ATM gene in breast cancer

Yong Jie Lu, Alison Condie, Julie D. Bennett, Michael J. Fry, Martin R. Yuille, Janet Shipley

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Mutations in the ATM gene, which maps to 11q22-23, cause the multisystem recessive syndrome ataxia-telangiectasia (AT). Breast cancer has been reported in AT patients and carriers. Sporadic breast cancer is associated with loss of heterozygosity at or in the region of ATM and chromosomal abnormalities involving 11q23. We have investigated the chromosomes, nuclei and released chromatin fibers from nine primary breast carcinoma and eight cell lines by fluorescence in situ hybridization with four fluorochrome-labeled cosmids spanning the ATM gene. The ATM gene was disrupted in one primary breast carcinoma and in the cell lines MDA-MB-231 and MCF-7. The role of these aberrations in breast carcinomas, which may lead to gene dosage or dominant negative effects on gene function, requires further investigation. © 2001 Elsevier Science Inc.
    Original languageEnglish
    Pages (from-to)97-101
    Number of pages4
    JournalCancer Genetics and Cytogenetics
    Volume126
    Issue number2
    DOIs
    Publication statusPublished - 15 Apr 2001

    Keywords

    • Ataxia Telangiectasia
    • Breast Neoplasms
    • Cell Cycle Proteins
    • Chromosome Aberrations
    • Chromosomes,Human,Pair 11
    • DNA-Binding Proteins
    • Female
    • genetics
    • Humans
    • In Situ Hybridization,Fluorescence
    • Loss of Heterozygosity
    • Mutation
    • Protein-Serine-Threonine Kinases
    • Proteins
    • Tumor Suppressor Proteins

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