DNA double-strand breaks: signaling, repair and the cancer connection View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2001-03

AUTHORS

Kum Kum Khanna, Stephen P. Jackson

ABSTRACT

To ensure the high-fidelity transmission of genetic information, cells have evolved mechanisms to monitor genome integrity. Cells respond to DNA damage by activating a complex DNA-damage-response pathway that includes cell-cycle arrest, the transcriptional and post-transcriptional activation of a subset of genes including those associated with DNA repair, and, under some circumstances, the triggering of programmed cell death. An inability to respond properly to, or to repair, DNA damage leads to genetic instability, which in turn may enhance the rate of cancer development. Indeed, it is becoming increasingly clear that deficiencies in DNA-damage signaling and repair pathways are fundamental to the etiology of most, if not all, human cancers. Here we describe recent progress in our understanding of how cells detect and signal the presence and repair of one particularly important form of DNA damage induced by ionizing radiation-the DNA double-strand break (DSB). Moreover, we discuss how tumor suppressor proteins such as p53, ATM, Brca1 and Brca2 have been linked to such pathways, and how accumulating evidence is connecting deficiencies in cellular responses to DNA DSBs with tumorigenesis. More... »

PAGES

ng0301_247

References to SciGraph publications

  • 2000-05. ATM-dependent phosphorylation of nibrin in response to radiation exposure in NATURE GENETICS
  • 2000-03. DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation in NATURE
  • 2000-10. Defying death after DNA damage in NATURE
  • 1999-11. ATM: A mediator of multiple responses to genotoxic stress in ONCOGENE
  • 1999-06. Mutations in the RAD54 recombination gene in primary cancers in ONCOGENE
  • 1999-06. Mutations of a novel human RAD54 homologue, RAD54B, in primary cancer in ONCOGENE
  • 2000-04. ATM phosphorylates p95/nbs1 in an S-phase checkpoint pathway in NATURE
  • 1997-04. Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2 in NATURE
  • 2000-03. hCds1-mediated phosphorylation of BRCA1 regulates the DNA damage response in NATURE
  • 1999-06. Mutant p53 proteins stimulate spontaneous and radiation-induced intrachromosomal homologous recombination independently of the alteration of the transactivation activity and of the G1 checkpoint in ONCOGENE
  • 2000-04. Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development in NATURE
  • 1999-04. DNA repair: Gatekeepers of recombination in NATURE
  • 2000-05. ATM phosphorylation of Nijmegen breakage syndrome protein is required in a DNA damage response in NATURE
  • 2000-03. A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage in NATURE
  • 2000-06. Frequent chromosomal translocations induced by DNA double-strand breaks in NATURE
  • 1999-05. Conditional mutation of Brca1 in mammary epithelial cells results in blunted ductal morphogenesis and tumour formation in NATURE GENETICS
  • 1997-07. Partial rescue of Brca15–6 early embryonic lethality by p53 or p21 null mutation in NATURE GENETICS
  • 2000-05. Functional link between ataxia-telangiectasia and Nijmegen breakage syndrome gene products in NATURE
  • Journal

    TITLE

    Nature Genetics

    ISSUE

    3

    VOLUME

    27

    Author Affiliations

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/85798

    DOI

    http://dx.doi.org/10.1038/85798

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1036425682

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/11242102


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