NDLI: 53BP1 and p53 synergize to suppress genomic instability and lymphomagenesis

Content Provider	PubMed Central
Author	Morales, Julio C. Franco, Sonia Murphy, Michael M. Bassing, Craig H. Mills, Kevin D. Adams, Melissa M. Walsh, Nicole C. Manis, John P. Rassidakis, George Z. Alt, Frederick W. Carpenter, Phillip B.
Copyright Year	2006
Abstract	p53-binding protein 1 (53BP1) participates in the cellular response to DNA double-stranded breaks where it associates with various DNA repair/cell cycle factors including the H2AX histone variant. Mice deficient for 53BP1 (53BP1 −/−) are sensitive to ionizing radiation and immunodeficient because of impaired Ig heavy chain class switch recombination. Here we show that, as compared with p53 −/− mice, 53BP1 −/−/p53 −/− animals more rapidly develop tumors, including T cell lymphomas and, at lower frequency, B lineage lymphomas, sarcomas, and teratomas. In addition, T cells from animals deficient for both 53BP1 and p53 (53BP1 −/−/p53 −/−) display elevated levels of genomic instability relative to T cells deficient for either 53BP1 or p53 alone. In contrast to p53 −/− T cell lymphomas, which routinely display aneuploidy but not translocations, 53BP1 −/−/p53 −/− thymic lymphomas fall into two distinct cytogenetic categories, with many harboring clonal translocations (40%) and the remainder showing aneuploidy (60%). We propose that 53BP1, in the context of p53 deficiency, suppresses T cell lymphomagenesis through its roles in both cell-cycle checkpoints and double-stranded break repair.
Related Links	http://dx.doi.org/10.1073/pnas.0511259103
Ending Page	3315
Page Count	6
Starting Page	3310
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	9
Volume Number	103
Language	English
Publisher	National Academy of Sciences
Publisher Date	2006-02-28
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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