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. 2002 Jun 28;109(7):811-21.
doi: 10.1016/s0092-8674(02)00770-5.

V体育平台登录 - Unrepaired DNA breaks in p53-deficient cells lead to oncogenic gene amplification subsequent to translocations

Chengming Zhu  1 , Kevin D Mills, David O Ferguson, Charles Lee, John Manis, James Fleming, Yijie Gao, Cynthia C Morton, Frederick W Alt
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Unrepaired DNA breaks in p53-deficient cells lead to oncogenic gene amplification subsequent to translocations

Chengming Zhu et al. Cell. .
Free article

Abstract (VSports app下载)

Amplification of large genomic regions associated with complex translocations (complicons) is a basis for tumor progression and drug resistance. We show that pro-B lymphomas in mice deficient for both p53 and nonhomologous end-joining (NHEJ) contain complicons that coamplify c-myc (chromosome 15) and IgH (chromosome 12) sequences. While all carry a translocated (12;15) chromosome, coamplified sequences are located within a separate complicon that often involves a third chromosome. Complicon formation is initiated by recombination of RAG1/2-catalyzed IgH locus double-strand breaks with sequences downstream of c-myc, generating a dicentric (15;12) chromosome as an amplification intermediate. This recombination event employs a microhomology-based end-joining repair pathway, as opposed to classic NHEJ or homologous recombination. These findings suggest a general model for oncogenic complicon formation VSports手机版. .

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