The common biology of cancer and ageing
By Toren Finkel, Manuel Serrano, M. Blasco. Nature, 2007
978 citations recorded by the source corpus.
Subfields: Aging, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/93dc788f051d1e70d033f386d34e89dfcc8d0e28
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Citations in the corpus
- Hypoxia and cancer (2007, background): “Although some cancers occur in the young, most are associated with the elderly, and both events represent the accumulation of genetic and epigenetic cell damage [2].”
- Linking functional decline of telomeres, mitochondria and stem cells during ageing (2010, neutral): “Studies in organisms ranging from yeast to primates have highlighted the importance of metabolic flux through the phosphatidylinositol-3-OH kinase (PI(3)K) pathway, as well as the activity of the master metabolic regulators such as sirtuins, the preservation of genome integrity by means of an effici”
- The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (2010, background): “In addition, these molecules can enhance cancer cell aggressiveness and can promote aging and age-related degeneration (96, 97).”
- Telomeres: Linking stress and survival, ecology and evolution (2010, background): “This pattern is also seen in human patients who have inherited genetic defects that limit telomere maintenance increasing their risk to a number of diseases (Finkel et al., 2007).”
- Obesity accelerates epigenetic aging of human liver (2014, background): “Aging and cancer are not only intricately linked to each other (30, 31) but also to obesity and metabolic syndrome (32).”
- Senescence-messaging secretome: SMS-ing cellular stress (2009, background): “Furthermore, senescence may have important implications for agein”
- Age and Cancer Risk (2014, neutral): “Whether the relationship between age and cancer risk is due primarily to the timedependent accumulation of genetic and epigenetic mutations or to an increased susceptibility of older adults to oncogenic mutations is not fully understood.(30,31) The multifactorial process of transformation from norma”
- The evolution of senescence from a comparative perspective (2008, background): “Indeed, several investigators have suggested a direct trade-off between the proliferation capacity of tissues, which tend to reduce ageing and tumour formation, which represents the uncontrolled proliferation of cells (Finkel et al. 2007).”
- Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. (2008, background): “However, this capacity comes at a cost because tissue renewal sets the stage for unscheduled proliferation upon the acquirement of oncogenic lesions (Finkel et al., 2007).”
- Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “These molecules can enhance cancer cell aggressiveness, as well as promote aging and age-related degeneration [70, 71].”
- Role of autophagy in cancer (2007, background): “Interestingly, autophagy is associated with longevity, suggesting a role in the suppression of ageing phenotype”