Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors.
By J. Campisi. Cell, 2005
2,340 citations recorded by the source corpus.
Subfields: Aging, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/2b8cb09e4e61fa774cf86ed13a0e717f15d24667
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Aging
In Molecular Biology
In Physiology
Citations in the corpus
- Kin Selection and the Evolutionary Theory of Aging (2007, background): “Related studies have provided better support for antagonistic pleiotropy than for mutation accumulation as genetic routes to aging (e.g., Campisi 2005, Hughes & Reynolds 2005, Kirkwood & Austad 2000, Leroi et al. 2005, Partridge & Barton 1993, Partridge & Gems 2002a, Rose 1991), with some phenomena…”
- Sirtuins: critical regulators at the crossroads between cancer and aging (2007, background): “While senescence protects against tumor development earlier in life, senescent cells may contribute to aging and agerelated diseases, such as cancer, by compromising tissue renewal and repair (Campisi, 2005).”
- The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “Blocking normal cells in G1 phase can protect them from drugs that target dividing cells (Carvajal et al. 2005; Kranz and Dobbelstein 2006).”
- Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “Senescent cells can accumulate with age and at sites of age-related pathologies, such as in osteoarthritis (261) and atherosclerosis (47), and can have an impact on the normal physiology of the tissues, causing a progressive functional deterioration.”