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Open Access Green as soon as Postprint is submitted to ZB.
Hyper-recombination and genetic instability in BLM-deficient epithelial cells.
Cancer Res. 63, 8578-8581 (2003)
Genetic instability appears to be required for a normal colorectal epithelial cell to evolve into a cancerous one. Bloom syndrome patients have a strong predisposition to cancer that affects a variety of tissues. The mechanism of disease is attributed to genomic instability, but many questions about the nature of this instability have not yet been answered. To investigate these issues, we used gene-targeting techniques to disrupt the BLM gene in karyotypically stable colorectal cancer epithelial cells. BLM knockout cells showed an increased tendency of sister chromatids to exchange DNA strands and were substantially more likely to undergo homologous recombination at chromosomal loci than parental cells. Surprisingly, BLM-deficient colorectal cancer epithelial cells did not display gross chromosomal rearrangements nor a change in the rates of chromosome gains and losses. However, the enhanced homologous recombination was associated with losses of heterozygosity. These observations define a type of genetic instability that has significant implications for the evolution of cancer.
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Publication type
Article: Journal article
Document type
Scientific Article
ISSN (print) / ISBN
0008-5472
e-ISSN
1538-7445
Journal
Cancer Research
Quellenangaben
Volume: 63,
Issue: 24,
Pages: 8578-8581
Publisher
American Association for Cancer Research (AACR)
Publishing Place
Philadelphia, Pa.
Reviewing status
Peer reviewed
Institute(s)
Institute of Human Genetics (IHG)