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

By R. D. Micco, M. Fumagalli, Angelo Cicalese, S. Piccinin, P. Gasparini, Chiara Luise, C. Schurra, M. Garrè, P. Nuciforo, A. Bensimon and 3 more. Nature, 2006

1,888 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e55bb1dcdd3af9accd668d382372804361acb207

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. J. Campisi
2. Jesús Gil
3. Adam Freund
4. F. Rodier
5. Manuel Serrano
6. D. Peeper
7. T. Kuilman
8. Zhijian J. Chen

In Physiology

1. J. Campisi
2. Jesús Gil
3. Adam Freund
4. Manuel Serrano
5. M. Demaria
6. F. Rodier
7. P. Desprez
8. Nicolás Herranz

Citations in the corpus

• mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype (2015, positive): “12 ) and the persistent DNA damage response associated with senescence 13 contribute to SASP induction 14 .”
• Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “Using the FUCCI reporter system to monitor cycle stages in live human cells, Nakanishi and colleagues recently found that senescence stimuli leading to a DDR can also result in “skipped” mitosis and a G1 arrest with 4N DNA content [12].”
• Nucleotide Deficiency Promotes Genomic Instability in Early Stages of Cancer Development (2011, background): “More recently, genomic instability in early cancer stages was shown to be caused by stress on the DNA replication, conferred by oncogene expression (Bartkova et al., 2006; Di Micco et al., 2006).”
• The essence of senescence. (2010, background): “The DDR and p53 often function in a common signal transduction cascade in which interference with specific DDR components can substitute for the loss of p53 function (Bartkova et al. 2006; Di Micco et al. 2006; Moiseeva et al. 2006; Mallette et al. 2007; Kim et al. 2009; Santoriello et al. 2009).”
• Mitochondrial dysfunction in cell senescence and aging (2022, background): “Such stresses often, but not always, involve a persistent DNA damage response (7).”
• DNA replication stress as a hallmark of cancer. (2015, background): “The ability of oncogenes to induce DNA replication stress has been well documented in tissue culture systems (62, 63).”
• Mechanisms and functions of cellular senescence. (2018, neutral): “In response to mitotic signals, an increase in usage of DNA replication origins leads to accumulation of genomic damage and activation of a DDR because of stalled replication forks (9, 28, 29).”