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

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  • 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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