In Spring 2021, I took the Cancer Biology course and had further understanding about the relationships between cancer and telomere. I used to think programmed cell death is a bad idea because it is not fair for those cells to die for the whole body. However, I realized that I cannot use human moral perspective to look at individual bodies. I like to connect the idea of biology and society together to see the similarities, such as if the human body is a city or a country, all the cells inside are like the citizens and residents. Cells work for the body and keep the body surviving, which is like citizens and residents do for the city and country. Therefore, it is cruel to kill them just because they are different from others.
Cancer cells need a plenty of time to mutate in the right order and they constantly experience the environmental stress. They are like someone taking advantages from the bodies and having more abilities to survive. However, they are not actively want to harm the body since a large portion of them is mutated by the environment and dysfunctional cells. Telomere could be considered a protective mechanism to avoid cells to replicate unlimitedly. It shorten its length each division, and make cells undergo senescence when the length of telomere is criticial short. Cancer cells are able to elongated the telomere to perform immortality, which is prohibied in any other adult cells. If we can borrow the idea of how cancer cells learn how to survive, maybe longer lifespan is at our fingertips. I think an improtant idea of our bodies is constantly doing the tradeoff between aging and avoiding cancer, which I acquired from the cancer biology course. However, aging and cancer have some similarities since cancer is a age-associated disease. As we aged, our bodies would make more mistakes, which no longer can be repaired, and can contribute to cancer. Meanwhile, telomere is also associated with aging as well. I doubt that telomere might be the key for both cancer and aging because of the protective property of telomere.
Recent years, it is believed that telomere length may be corelated to the longevity. However, The lengths of telomere are varied between species. The activities of the enzyme, telomerase, which is silenced in adult cells but active in fetal cells, are also varied between species as well. Therefore, the longer of the lengths of telomeres does not indicate the longer lifespan generally. For instance, mice have longer telomeres (25-150 kb) compared with humans (15-20 kb) (Gomes et al., 2011). Moreover, mouse telomeres shorten ∼100 times faster than human telomeres (Vera et al., 2012), which makes the lengths of telomere not directly corelated to life span. Interestingly, the telomerase is active constitutively in most mice cells, which suggests that the results we examined from mice might not be necessarily observed in human.
It has not been more than thirty to forty years since telomeres and telomerases were discovered. Commercially, there are many medicine and therapies claim that they could regrow or repair the shorten telomeres. However, the longer the telomere length does not indicate the healthier of the bodies. Even though many studies showed short telomeres have high incidence of cancer, activate the telomerase might not be a good idea since the telomerase also increase the chance of getting cancer. Interestingly, high telomerase activities do not equal to high transformational rates. If there is no chromosomal instability, high telomerase activities might not be an issue; if the telomeres could be elongated before reach their limits, chromatid fusions might not be an issue; if the p53 is not loss, all of above including breakage-fusion-bridge cycle will not even be able to transform cells. It is important to recognize that not any single mutation could cause cancer. Sometimes, those mutations even must come in order to end with an individual viable cancer cell. For instance, what will happen if the reawaken telomerase come first before any other mutations? In the hyper-long telomere mice experiment, even the mice have constitutive telomerases, the hyper-long telomeres still protect them from getting cancer. Maybe the telomeres were too long, so no chromatid fusion could occur since the telomeres never have chance to shorten enough in their relatively short lifespan?
Reference:
Gomes, N. M. et al. (2011). Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination. Aging Cell 10, 761–768. https://doi.org/10.1111/j.1474-9726.2011.00718.x
Vera, E., et al. (2012). The rate of increase of short telomeres predicts longevity in mammals. Cell Rep. 2, 732–737. https://doi.org/10.1016/j.celrep.2012.08.023