Living on a break: cellular senescence as a DNA-damage response

By F. d’Adda di Fagagna. Nature Reviews. Cancer, 2008

1,004 citations recorded by the source corpus.

Subfields: Dermatology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/49a9bb1241acf5284c1838ad6579bd4d59b01b49

How researchers see this paper

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

In Dermatology

1. J. Campisi
2. Manuel Serrano
3. C. Abate-Shen
4. D. Meek
5. Rafik Amir Salama
6. M. Shen
7. P. Jat
8. D. Peeper

In Molecular Biology

1. J. Campisi
2. M. Demaria
3. Adam Freund
4. Manuel Serrano
5. D. Peeper
6. T. Kuilman
7. P. Desprez
8. Jean-Philippe Coppé

In Physiology

1. J. Campisi
2. M. Demaria
3. Adam Freund
4. Manuel Serrano
5. P. Desprez
6. D. Peeper
7. T. Kuilman
8. Jean-Philippe Coppé

Citations in the corpus

• Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “Cellular senescence corresponds to a form of cell cycle arrest in which cells remain fully viable, but are nonproliferative despite exposure to mitogenic signals (Courtois-Cox et al. 2008; d'Adda di Fagagna 2008; Evan and d'Adda di Fagagna 2009).”
• The essence of senescence. (2010, background): “The factors bringing about this differential outcome have remained largely elusive, but the cell type and the intensity and duration of the signal, as well as the nature of the damage, are likely to be important determinants (D’Adda di Fagagna 2008).”
• Inflammatory Networks during Cellular Senescence: Causes and Consequences (2010, background): “In the case of senescence, cells arrest growth and maintain chronic low-level DDR signaling [57].”
• Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “Thus, while the DDR is important, it is not sufficient; there must be other, slower events that cooperate with the DDR to induce the SASP.”
• Cellular Senescence: Defining a Path Forward. (2019, positive): “This response can also be elicited by inhibiting or altering genes involved in telomere maintenance (d’Adda di Fagagna, 2008).”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “However, diploid cells can also experience an accelerated senescence response, independent from the telomere shortening, known as premature senescence (79, 82, 283).”
• Cellular senescence and its effector programs (2014, methodology): “…the exact threshold of telomere length or the number of dysfunctional telomeres within a cell that can trigger senescence is still unclear (d’Adda di Fagagna 2008), 100 GENES & DEVELOPMENT a current structural model describes three states of telomeres: closed state (t-loop formed), intermediate…”