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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.

Author information

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

Abstract

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.

PMID:
17980599
[PubMed - indexed for MEDLINE]
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