DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-04

AUTHORS

Jirina Bartkova, Zuzana Hořejší, Karen Koed, Alwin Krämer, Frederic Tort, Karsten Zieger, Per Guldberg, Maxwell Sehested, Jahn M. Nesland, Claudia Lukas, Torben Ørntoft, Jiri Lukas, Jiri Bartek

ABSTRACT

During the evolution of cancer, the incipient tumour experiences 'oncogenic stress', which evokes a counter-response to eliminate such hazardous cells. However, the nature of this stress remains elusive, as does the inducible anti-cancer barrier that elicits growth arrest or cell death. Here we show that in clinical specimens from different stages of human tumours of the urinary bladder, breast, lung and colon, the early precursor lesions (but not normal tissues) commonly express markers of an activated DNA damage response. These include phosphorylated kinases ATM and Chk2, and phosphorylated histone H2AX and p53. Similar checkpoint responses were induced in cultured cells upon expression of different oncogenes that deregulate DNA replication. Together with genetic analyses, including a genome-wide assessment of allelic imbalances, our data indicate that early in tumorigenesis (before genomic instability and malignant conversion), human cells activate an ATR/ATM-regulated DNA damage response network that delays or prevents cancer. Mutations compromising this checkpoint, including defects in the ATM-Chk2-p53 pathway, might allow cell proliferation, survival, increased genomic instability and tumour progression. More... »

PAGES

864

References to SciGraph publications

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  • Journal

    TITLE

    Nature

    ISSUE

    7035

    VOLUME

    434

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature03482

    DOI

    http://dx.doi.org/10.1038/nature03482

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1037091000

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/15829956


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