Frequently attributed to the multi-hit hypothesis and the time required to accumulate genomic mutations, this question is a matter of ongoing debate.
Here, we propose that the normal decline in oxidative metabolism during aging constitutes an early and important “hit” that drives tumorigenesis.
Central to these metabolic changes are the sirtuins, a family of NAD+-dependent deacylases that have evolved as coordinators of physiological responses to nutrient intake and energetic demand.
Thus, the modulation of sirtuins might be a fruitful approach to reversing the age-related metabolic changes that could underlie tumorigenesis."
Geroncogenesis: Metabolic Changes during Aging as a Driver of Tumorigenesis
Lindsay E. Wu Ana P. Gomes David A. Sinclair
https://www.cell.com/cancer-cell/fullte ... 13)00534-5
"Increasing NAD+ levels has been shown to protect mice from metabolic decline in mouse models of obesity and aging (Cantó et al., 2012, Escande et al., 2013, Yoshino et al., 2011), but it is not yet considered a viable strategy for cancer, in part because raising overall NAD+ levels is not without risks.
As described above, there is evidence that SIRT1 and SIRT7 may promote the growth of cancers. It is also important to consider the role of NAD+ as a redox carrier that is essential to glycolysis, which cancer cells heavily rely upon.
Another consideration is the fact that raising NAD+ may not be as simple as it sounds. NAD+ is compartmentalized into cytosolic, nuclear, and mitochondrial pools (Nikiforov et al., 2011), and it is unclear what degree of flux exists between these pools and whether a particular pool of NAD+ influences the Warburg effect and tumorigenesis."