Outside of cancer biology, normal, well-behaved cells undergo a finite number of cell divisions. This is thought to be a general anti-cancer mechanism, since tired, older cells with metabolic dysfunction and increased exposure to environmental toxins- if they were to divide- are more likely to accumulate, and pass on mutations that cold promote the development of cancer. Because senescent cells have permanently exited the cell cycle, they are no longer at risk for passing along potentially harmful DNA mutations to daughter cells, potentially reducing cancer risk.[1]
However, cellular senescence can be a double-edged sword. Senescent cells tend to develop pro-inflammatory characteristics, constantly secreting low-levels of pro-inflammatory molecules. This phenomenon has been called SASP (Senescence-associated secretory phenotype). Although senescent cells with SASP are at a lower risk for developing into tumors themselves, their tendency create a pro-inflammatory tissue microenvironment in/around their non-senescent neighbors has been implicated in NAD+ depletion [2] and potentially the development of cancer in neighboring cells.[3]