期刊
ANNUAL REVIEW OF IMMUNOLOGY, VOL 29
卷 29, 期 -, 页码 319-350出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-immunol-031210-101329
关键词
antigen receptor genes; DNA double-strand breaks; nonhomologous end-joining; DSB repair; lymphoma
类别
资金
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
- NCI NIH HHS [5P01 CA92625-09, P01 CA109901, 5P01 CA109901-05] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA109901, P01CA092625] Funding Source: NIH RePORTER
Recurrent chromosomal translocations are characteristic features of many types of cancers, especially lymphomas and leukemias. Several basic mechanistic factors are required for the generation of most translocations. First, DNA double-strand breaks (DSBs) must be present simultaneously at the two participating loci. Second, the two broken loci must either be in proximity or be moved into proximity to be joined. Finally, cellular DNA repair pathways must be available to join the two broken loci to complete the translocation. These mechanistic factors can vary in different normal and mutant cells and, as a result, substantially influence the frequency at which particular translocations are generated in a given cell type. Ultimately, however, appearance of recurrent oncogenic translocations in tumors is, in most cases, strongly influenced by selection for the translocated oncogene during the tumorigenesis process. In this review, we discuss in depth the factors and pathways that contribute to the generation of translocations in lymphocytes and other cell types. We also discuss recent findings regarding mechanisms that underlie the appearance of recurrent translocations in tumors.
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