| Literature DB >> 17980599 |
Raffaella Di Micco1, Marzia Fumagalli, Fabrizio d'Adda di Fagagna.
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.Entities:
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Year: 2007 PMID: 17980599 DOI: 10.1016/j.tcb.2007.07.012
Source DB: PubMed Journal: Trends Cell Biol ISSN: 0962-8924 Impact factor: 20.808