EMBO J 31 13, 2839–2851 (2012); published online May 08 2012 Senescence represents a major tumour suppressor checkpoint activated by telomere dysfunction or cellular stress factors such as oncogene activation. In this issue of , Suram et al (2012) reveal a surprising interconnection between oncogene activation and telomere dysfunction induced senescence. The study supports an alternative model of tumour suppression, indicating that oncogene-induced accumulation of telomeric DNA damage contributes to the induction of senescence in telomerase-negative tumours.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3395100 | PMC |
http://dx.doi.org/10.1038/emboj.2012.162 | DOI Listing |
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