Aging and cancer have evolved hand in hand, and numerous aspects of our biology play an important role in both. At the simplest, highest level we have things like the decline in stem cell activity and tissue maintenance with age as a part of the evolution of human life span as a balance between death by cancer and death by functional failure of organs. There is also the role of senescent cells in both suppressing and promoting cancer, and their accumulation as a cause of degenerative aging. There are many other more complex and less well understood relationships between aging and cancer, but this review focuses largely on cellular senescence as a comparatively new area for building interventions:
A growing body of evidence supports the view that the complex relationship between mechanisms underlying aging and cancer evolves with organismal chronological age. Significant progress has been made in defining cell-autonomous and cell-nonautonomous mechanisms that in young and adult organisms simultaneously delays aging and suppress tumor formation. Furthermore, it is now well established that the intricate interplay between mechanisms underlying aging and cancer reflects the proliferative history of cells and is impacted by the progression of a cellular senescence program. Recent findings imply that the advancement of the multistep cellular senescence program imposes antagonistically pleiotropic effects on aging and cancer.
Despite an important conceptual advance in our understanding of the complex interplay between mechanisms underlying aging and cancer, we are still lacking answers to the following fundamentally important questions. Which of the numerous morphological and functional changes observed in various types of senescent cells in culture and in vivo are universal hallmarks of a state of cellular senescence - and, thus, which of these changes can be used as diagnostic biomarkers of cells entered such a state in any tissue? Given that the progression of the cellular senescence program imposes antagonistically pleiotropic effects on aging and cancer what therapeutic interventions have a potential to be used not only for enhancing those effects that are anti-aging and/or anti-cancer but also for attenuating those effects that are pro-aging and/or pro-cancer?
Recent findings in mice engineered for a reversal of the cellular senescence state by a drug-inducible telomerase reactivation or for a late-life immune clearance of senescent cells by their drug-inducible elimination suggest that small chemicals can be used for: (1) a protein target-specific pharmacological enhancement of the beneficial for organismal healthspan effects imposed by the cellular senescence program; and/or (2) a protein target-specific pharmacological attenuation of the deleterious for organismal healthspan effects inflicted by this program.