“Bypassed stasis” is a term often used in the context of cellular senescence and cell culture. Cellular senescence is a state of permanent cell cycle arrest, which cells can enter in response to a variety of stress signals, including telomere shortening, DNA damage, and oncogenic signaling. Senescent cells cannot divide, but they remain metabolically active and can secrete a variety of factors that can affect the surrounding tissue environment.

In cell culture, normal human cells can replicate only a limited number of times before they enter a state of senescence, often referred to as “replicative senescence” or “stasis.” This limit is also known as the Hayflick limit, named after Leonard Hayflick who first described this phenomenon in the 1960s.

However, under certain conditions, cells can bypass this senescent state and continue to proliferate. This is often referred to as “bypassed stasis” or “crisis bypass.” For example, cells that have mutations in certain genes, such as the tumor suppressor genes p53 and Rb, are often able to bypass senescence. Similarly, cells that re-activate telomerase, an enzyme that adds DNA to the ends of chromosomes and counteracts telomere shortening, can also bypass senescence.

Bypassing stasis can allow cells to continue dividing indefinitely, leading to a state of “immortalization.” However, this can also lead to genomic instability and has been associated with the development of cancer. In fact, most cancer cells have bypassed senescence and have the ability to proliferate indefinitely.