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Trends Cell Biol. 2007 Nov;17(11):529-36. Epub 2007 Nov 5.

Breaking news: high-speed race ends in arrest--how oncogenes induce senescence.

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  • 1IFOM Foundation - FIRC Institute of Molecular Oncology Foundation, via Adamello 16, 20139 Milan, Italy.


Oncogene activation in normal cells induces a permanent proliferative arrest known as cellular senescence. This phenomenon restrains the expansion of cells that bear an activated oncogene and acts as a powerful tumor-suppressive process. Although the full molecular mechanisms are still being elucidated, it has been observed recently that some oncogenes alter the DNA-replication process and cause DNA-damage accumulation. DNA-damage checkpoint-response activation together with the increased appearance of heterochromatin formation that leads to transcriptional silencing of proliferative genes are, presently, the two main mechanisms known that establish and maintain oncogene-induced senescence. Here, we discuss the most recent advancements in understanding the molecular and cellular mechanisms that control cellular senescence caused by oncogene activation and their impact on cancer studies.

[PubMed - indexed for MEDLINE]
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