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Cited by 320

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Gross chromosomal rearrangements and genetic exchange between nonhomologous chromosomes following BRCA2 inactivation

Open access
Yu, Veronica P.C.C., Koehler, Michael, Steinlein, Claus, Schmid, Michael, Hanakahi, Leslyn A., van Gool, Alain J., West, Stephen C., Venkitaraman, Ashok R.·2000·Genes & Development

Abstract

Cancer-causing mutations often arise from gross chromosomal rearrangements (GCRs) such as translocations, which involve genetic exchange between nonhomologous chromosomes. Here we show that murine Brca2 has an essential function in suppressing GCR formation after chromosome breakage. Cells that harbor truncated Brca2 spontaneously incur GCRs and genomic DNA breaks during division. They exhibit hypersensitivity to DNA damage by interstrand cross-linkers, which even at low doses trigger aberrant genetic exchange between nonhomologous chromosomes. Therefore, genetic instability in Brca2-deficient cells results from the mutagenic processing of spontaneous or induced DNA damage into gross chromosomal rearrangements, providing a mechanistic basis for cancer predisposition.

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Crossref · 10.1101/gad.14.11.1400

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Metadata

Authors
Yu, V. P. C. C., Koehler, M., Steinlein, C., Schmid, M., Hanakahi, L. A., van Gool, A. J., West, S. C., & Venkitaraman, A. R.
Venue
Genes & Development
Published
2000-06-01
Volume
14
Issue
11
Pages
1400-1406
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2136989353
Cited by
320
References
3
Type
posted content
Language
en
Open access
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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