Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints

@article{Brtkov2006OncogeneinducedSI,
  title={Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints},
  author={Jiřina B{\'a}rtkov{\'a} and Nousin Rezaei and Michalis Liontos and Panagiotis Karakaidos and Dimitris Kletsas and Natalia Issaeva and Leandros V Vassiliou and Evangelos Kolettas and Katerina Niforou and Vassilis Zoumpourlis and Munenori Takaoka and Hiroshi Nakagawa and Frederic Tort and Kasper Fugger and Fredrik I Johansson and Maxwell Sehested and Claus Lindbjerg Andersen and Lars Dyrskj{\o}t and Torben F. {\O}rntoft and Jiri Lukas and Christos N. Kittas and Thomas Helleday and Thanos D Halazonetis and Jiri Bartek and Vassilis G. Gorgoulis},
  journal={Nature},
  year={2006},
  volume={444},
  pages={633-637}
}
Recent studies have indicated the existence of tumorigenesis barriers that slow or inhibit the progression of preneoplastic lesions to neoplasia. One such barrier involves DNA replication stress, which leads to activation of the DNA damage checkpoint and thereby to apoptosis or cell cycle arrest, whereas a second barrier is mediated by oncogene-induced senescence. The relationship between these two barriers, if any, has not been elucidated. Here we show that oncogene-induced senescence is… 

Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication

TLDR
It is shown that senescence, triggered by the expression of an activated oncogene (H-RasV12) in normal human cells, is a consequence of the activation of a robust DDR, and proposed that OIS results from the enforcement of a DDR triggered by oncogen-induced DNA hyper-replication.

The DNA Damage Signaling Pathway Connects Oncogenic Stress to Cellular Senescence

TLDR
Evidence indicating that oncogene induced senescence (OIS) involves activation of p53 via the DNA damage response (DDR) is reviewed, which implies mechanisms of DNA damage in cells expressing oncogenes, that may be secondary to reactive oxygen species and/or some form of “oncogenic stress” that affect normal DNA replication.

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TLDR
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TLDR
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TLDR
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TLDR
Recent advances in understanding of molecular mechanisms leading to hyper-replication stress in response to oncogene activation, and of the crosstalk between replication stress and persistent activation of the DNA damage response (DDR) pathway are highlighted.

Enhanced elimination of oxidized guanine nucleotides inhibits oncogenic RAS-induced DNA damage and premature senescence

TLDR
It is demonstrated that overexpression of MTH1 can prevent the oncogenic H-RAS-induced DDR and attendant premature senescence, although it does not affect the observed elevation in ROS levels produced by RAS oncoprotein expression.
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References

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It is shown that senescence, triggered by the expression of an activated oncogene (H-RasV12) in normal human cells, is a consequence of the activation of a robust DDR, and proposed that OIS results from the enforcement of a DDR triggered by oncogen-induced DNA hyper-replication.

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