Unrepaired DNA breaks in p53-deficient cells lead to oncogenic gene amplification subsequent to translocations.
Chengming Zhu,Kevin D. Mills,David O. Ferguson,Charles Lee,John P. Manis,James Fleming,Yijie Gao,Cynthia C. Morton,Frederick W. Alt +8 more
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TLDR
It is shown that pro-B lymphomas in mice deficient for both p53 and nonhomologous end-joining (NHEJ) contain complicons that coamplify c-myc and IgH sequences, suggesting a general model for oncogenic complicon formation.About:
This article is published in Cell.The article was published on 2002-06-28 and is currently open access. It has received 418 citations till now. The article focuses on the topics: Chromosome 12 & Microhomology-mediated end joining.read more
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Genomic Instability and Aging-like Phenotype in the Absence of Mammalian SIRT6
Raul Mostoslavsky,Katrin F. Chua,Katrin F. Chua,David B. Lombard,Wendy W. Pang,Miriam R. Fischer,Lionel Gellon,Pingfang Liu,Gustavo Mostoslavsky,Sonia Franco,Michael M. Murphy,Kevin D. Mills,Parin Patel,Joyce T. Hsu,Andrew L. Hong,Ethan Ford,Hwei Ling Cheng,Caitlin Kennedy,Nomeli P. Nunez,Nomeli P. Nunez,Roderick T. Bronson,David Frendewey,Wojtek Auerbach,David M. Valenzuela,Margaret Karow,Michael O. Hottiger,Stephen D. Hursting,J. Carl Barrett,J. Carl Barrett,Leonard Guarente,Richard C. Mulligan,Bruce Demple,George D. Yancopoulos,Frederick W. Alt +33 more
TL;DR: It is demonstrated that SIRT6 is a nuclear, chromatin-associated protein that promotes resistance to DNA damage and suppresses genomic instability in mouse cells, in association with a role in base excision repair (BER).
Journal ArticleDOI
MMEJ repair of double-strand breaks (director’s cut): deleted sequences and alternative endings
Mitch McVey,Sang Eun Lee +1 more
TL;DR: A mechanistic model for MMEJ is proposed and important questions for future research are highlighted, including how microhomology contributes to oncogenic chromosome rearrangements and genetic variation in humans.
Journal ArticleDOI
PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways
TL;DR: It is shown that PARP-1 operates in an alternative pathway of non-homologous end joining (NHEJ) that functions as backup to the classical pathway of NHEJ that utilizes DNA-PKcs, Ku, DNA ligase IV, XRCC4, XLF/Cernunnos and Artemis.
Journal ArticleDOI
Alternative-NHEJ is a mechanistically distinct pathway of mammalian chromosome break repair.
TL;DR: It is suggested that alt-NHEJ is a mechanistically distinct pathway of DSB repair, and thus may play a unique role in mutagenesis during cancer development and therapy.
Journal ArticleDOI
Telomeres and telomerase in cancer.
TL;DR: The role of telomeres and telomerase is covered in the biology of normal tissue stem/progenitor cells and in the development of cancer to uncover the underlying mechanisms driving genome instability in cancer.
References
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Molecular Cloning: A Laboratory Manual
TL;DR: Molecular Cloning has served as the foundation of technical expertise in labs worldwide for 30 years as mentioned in this paper and has been so popular, or so influential, that no other manual has been more widely used and influential.
Journal ArticleDOI
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Lawrence A. Donehower,Michele Harvey,Betty L. Slagle,Mark J. McArthur,Charles A. Montgomery,Janet S. Butel,Allan Bradley +6 more
TL;DR: Observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.
Journal ArticleDOI
Genetic instabilities in human cancers
TL;DR: There is now evidence that most cancers may indeed be genetically unstable, but that the instability exists at two distinct levels, and recognition and comparison of these instabilities are leading to new insights into tumour pathogenesis.
Journal ArticleDOI
Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification
Mercedes E. Gorre,Mansoor Mohammed,Katharine Ellwood,Nicholas C. Hsu,Ron Paquette,P. Nagesh Rao,Charles L. Sawyers +6 more
TL;DR: It is found that drug resistance is associated with the reactivation of BCR-ABL signal transduction in all cases examined and a strategy for identifying inhibitors of STI-571 resistance is suggested.
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