The human body is a factory producing trillions of new blood cells daily, and replacing the lining of the small intestine on a weekly basis. The raw materials in production are stem cells, which have the ability both to create cells used by our body, and to create copies of themselves.
To ensure quality of production, the body creates various quality control measures expressed in the form of proteins and caps on DNA which will either cause the cell to be killed and catabolized (apoptosis) or cause the cell to enter a state of permanent irreversible growth arrest (senescence). Accumulation of these “frozen” cells leads to the eventual aging of our bodies. On the other hand, if quality control measures fail, cells can become pathological, often proliferating without control in a phenomenon known as cancer.
The result can lead one to theorize a trade-off between aging and cancer as is proposed by Norman Sharpless and Ronald DePinho in the Stem Cell Theory of Aging. It is a tantalizing theory as expression of cancer suppressing mechanisms p53, p16Ink4a, and shortened telomeres, also appear in older cells and tissues. The correlation provides good motivation to increase understanding of how these cell cycle check points work. In the meantime, Sharpless and DePinho will use expression of these proteins in epidemiological research so that better associations between lifestyle, aging, and cancer can be made.
In my mind, their paper raises a number of intruiging questions:
- Why don’t cell cycle check points lead to apoptosis as opposed to senescence?
- Why does the amount of stem cells in our body decline over time?
- Are there potential drug targets in the cell cycle that can prevent both aging and cancer?
I will look forward to research with the answers.
Sharpless, N. (2004). Telomeres, stem cells, senescence, and cancer Journal of Clinical Investigation, 113 (2), 160-168 DOI: 10.1172/JCI200420761
Tags: Aging, apoptosis, cancer, senescence
