Cancer + Telomerase = Immortality?
Unlike cultures taken from other patients, the "HeLa" cells continued to divide and replicate indefinitely, thus becoming the first "immortal" cell line.
Cancer has been one of the leading causes of death in the United States for over 75 years according to the CDC, and has been extensively researched over this time as well. What was once thought to stem from coagulated lymph, the modern concepts of cancer physiology and causative factors have more recently unraveled in the 19th and 20th centuries, with notable scientific growth since the cultivation of Henrietta Lacks's "HeLa" cells in 1951.
At the time, Henrietta was just 31 years old when she passed away from cervical cancer at Johns Hopkins. While ethically questionable, the surgeon legally cultivated some of Henrietta's cancerous tissue without her or her family's consent, which was common practice at the time. Unlike cultures taken from other patients, the "HeLa" cells continued to divide and replicate indefinitely, thus becoming the first "immortal" cell line. Being that she was 31 at the time, these cells are roughly 104 years old by this point, but how exactly is it possible for human cells to become immortal?
A large portion of cancer physiology includes the disruption of normal cell division primarily caused by DNA mutations in key genes involved in genomic stability and protection. These could be categorized into three broad groups: tumor suppressor genes, proto-oncogenes, and DNA repair genes. Ultimately, cancer will alter normal physiology and do some incredibly interesting things that include but are not limited to the generation of new blood vessels (angiogenesis) supplying it with energy and nutrients, altering metabolic function (Warburg effect), and the ability to invade and metastasize. Most relevant to the immortality discussion is the activation of telomerase enzymes that function to maintain telomere length at the ends of each chromosome.
Telomeres normally act to help protect your genome and allow for cell division, though during each round of replication, the telomere will shorten until there is nothing left. Without telomeres, the cell will become senescent, which can lead to cellular death. A wonderful comparison to describe the function of these telomeres is imagining them as aglets, the plastic tips of your shoelace; without them, it leads to damage and fraying of the material and unfortunately, there isn't an equivalent cellular shoe store for your chromosomes to buy a replacement. Cancer cells bypass the loss of telomeres and eventual cell death by activating telomerase enzymes that build back telomere length and allow for indefinite cell replication or "immortality".
While this is just a small snippet of the greater picture relating to cell survival, cancer physiology, and immortality, it's still an interesting topic! I've quite literally fantasized about medicines centered around the elongation of telomeres to prolong the human lifespan since my latter years of high school. This idea of toying with telomerase expression isn't weightless, but wouldn't account for other cellular complications including oxidative stress and poor functionality. It also makes the assumption that the quality of life years would remain the same, which is highly unlikely. Would you want to gain an additional 10 or 20 years of life? In that context it seems to be an easy question, but what if your quality of life dropped to 50% of your baseline over that timeframe? I know that might change my answer!
References
- https://www.cdc.gov/nchs/hus/topics/cancer-deaths.htm#ref1
- https://aacrjournals.org/cancerres/article/68/17/6861/540601/The-History-of-Cancer-Research-Introducing-an-AACR
- https://www.hopkinsmedicine.org/henrietta-lacks
- https://aacrjournals.org/cancerdiscovery/article/12/1/31/675608/Hallmarks-of-Cancer-New-DimensionsHallmarks-of
- https://www.sciencedirect.com/topics/neuroscience/telomerase#:~:text=Telomerase%20is%20a%20reverse%20transcriptase%20that%20adds%20repeats%20of%20a,cell%20death%20(cellular%20senescence).
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