Cellular senescence in cancer and aging.
By M. Collado, M. Blasco, Manuel Serrano. Cell, 2007
1,708 citations recorded by the source corpus.
Subfields: Aging, Dermatology, Physiology
View Paper: https://www.semanticscholar.org/paper/895d85eb7d90317e4ffd6ec682836b6dd2e3247a
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Citations in the corpus
- Chemokine signaling via the CXCR2 receptor reinforces senescence. (2008, background): “Cellular senescence is therefore intimately associated with aging (Collado et al., 2007).”
- Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “All the abovementioned features define the gold-standard markers to identify senescent cells and represent the actual hallmarks of senescence (70, 157, 192).”
- Autophagy mediates degradation of nuclear lamina (2015, positive): “In fact, most primary cells and tissues cope with oncogenic Ras activity by inducing cellular senescence, a stable cell cycle arrest that serves as a potent tumor suppressive mechanism 20,21 .”
- Stem cells and niches: mechanisms that promote stem cell maintenance throughout life. (2008, background): “Mammalian stem cells have surveillance mechanisms that detect unresolved DNA damage and that eliminate the cells in which this occurs, possibly by activation of the tumor suppressor proteins p53 or Rb leading to senescence (Collado et al., 2007).”
- Oxidative Stress in Aging Human Skin (2015, background): “An activation of the senescence program leads to an irreversible cell-cycle arrest in the G1-phase [330,331].”
- Programmed cell senescence during mammalian embryonic development. (2013, positive): “notably within tumors and in some aged tissues (Campisi and d’Adda di Fagagna, 2007; Collado et al., 2007).”
- Induced pluripotency: history, mechanisms, and applications. (2010, result): “In contrast to ESCs, which are immortal, fibroblasts and most other somatic cell types have a restricted proliferative potential and undergo apoptosis, growth arrest, or stress-induced senescence in culture (Collado et al. 2007).”
- Senescence of activated stellate cells limits liver fibrosis (2008, background): “To identify senescent cells in situ, we stained liver sections from CCl4 and vehicle-treated (control) mice for a panel of senescence-associated markers, including SA-b-gal and proteins such as p16, p21, p53, and Hmga1, which have been causally linked to the senescence program (Collado et al., 2007;”