Loss of 53BP1 is a gain for BRCA1 mutant cells Journal Article


Authors: Kass, E. M.; Moynahan, M. E.; Jasin, M.
Article Title: Loss of 53BP1 is a gain for BRCA1 mutant cells
Abstract: Mutations in BRCA1 predispose to tumorigenesis presumably from the inability to accurately repair DNA double-strand breaks by homologous recombination. Two new papers shed light on how loss of the DNA damage response protein 53BP1 reverses phenotypes of BRCA1 mutant cells, with potential clinical implications. © 2010 Elsevier Inc. All rights reserved.
Keywords: signal transduction; unclassified drug; gene mutation; gene deletion; cisplatin; nonhuman; drug targeting; phenotype; homologous recombination; dna repair; cancer susceptibility; ovary cancer; breast cancer; nuclear protein; protein depletion; antineoplastic activity; mutational analysis; brca1 protein; carcinogenesis; cancer resistance; cancer genetics; short survey; chromosomal instability; nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase inhibitor; double stranded dna break; platinum derivative; protein 53bp1
Journal Title: Cancer Cell
Volume: 17
Issue: 5
ISSN: 1535-6108
Publisher: Cell Press  
Date Published: 2010-05-18
Start Page: 423
End Page: 425
Language: English
DOI: 10.1016/j.ccr.2010.04.021
PROVIDER: scopus
PUBMED: 20478525
DOI/URL:
Notes: --- - "Cited By (since 1996): 3" - "Export Date: 20 April 2011" - "CODEN: CCAEC" - "Source: Scopus"
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  1. Mary Ellen Moynahan
    105 Moynahan
  2. Maria Jasin
    249 Jasin
  3. Elizabeth M Kass
    13 Kass