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Telomeres<br />

WAYS TO<br />

PROLONG LIFE<br />

B y A n d r e w S t e fa n i<br />

Two hundred years ago, the average life<br />

expectancy oscillated between 30 and 40<br />

years, as it had for centuries before. Medical<br />

knowledge was fairly limited to superstition<br />

and folk cures, and the science behind what<br />

actually caused disease and death was lacking.<br />

Since then, the average lifespan of human<br />

beings has skyrocketed due to scientific<br />

advancements in health care, such as an<br />

understanding of bacteria and infections.<br />

Today, new discoveries are being made<br />

in cellular biology which, in theory, could<br />

lead us to the next revolutionary leap in life<br />

span. Most promising among these recent<br />

discoveries is the manipulation of telomeres<br />

in order to slow the aging process, and the<br />

use of telomerase to identify cancerous cells.<br />

Before understanding how telomeres can be<br />

utilized to increase the average lifespan of<br />

humans, it is essential to understand what<br />

a telomere is. When cells divide, their DNA<br />

must be copied so that all of the cells share<br />

an identical DNA sequence. However, the<br />

DNA cannot be copied all the way to the end<br />

of the strand, resulting in the loss of some<br />

DNA at the end of the sequence with every<br />

single replication. 1 To prevent valuable genetic<br />

code from being cut off during cell division,<br />

our DNA contains telomeres, a meaningless<br />

combination of nucleotides at the end of our<br />

chromosomal sequences that can be cut off<br />

without consequences to the meaningful<br />

part of the DNA. Repeated cell replication<br />

causes these protective telomeres to become<br />

shorter and shorter, until valuable genetic<br />

code is eventually cut off, causing the cell to<br />

malfunction and ultimately die. 1 The enzyme<br />

telomerase functions in cells to rebuild these<br />

constantly degrading telomeres, but its activity<br />

is relatively low in normal cells as compared to<br />

cancer cells. 2<br />

The applications of telomerase manipulation<br />

have only come up fairly recently, with<br />

the discovery of the functionality of both<br />

telomeres and telomerase in the mid 80’s<br />

by Nobel Prize winners Elizabeth Blackburn,<br />

Carol Grieder, and Jack Sjozak. 3 Blackburn<br />

discovered a sequence at the end of<br />

chromosomes that was repeated several<br />

times, but could not determine what the<br />

purpose of this sequence was. At the same<br />

time, Sjozak was observing the degradation of<br />

minichromosomes, chromatin-like structures<br />

which replicated during cell division when<br />

introduced to a yeast cell. Together, they<br />

combined their work by isolating Blackburn’s<br />

repeating DNA sequences, attaching them to<br />

Telomeres<br />

(Protective Caps)<br />

Paired Strands of<br />

DNA<br />

Figure 1: DNA strand with telomere ends<br />

Sjozak’s minichromosomes, and then placing<br />

the minichromosomes back inside yeast cells.<br />

With the new addition to their DNA sequence,<br />

the minichromosomes did not degrade as they<br />

had before, thus proving that the purpose<br />

of the repeating DNA sequence, dubbed the<br />

telomere, was to protect the chromosome and<br />

delay cellular aging.<br />

Because of the relationship between<br />

telomeres and cellular aging, many scientists<br />

theorize that cell longevity could be enhanced<br />

by finding a way to control telomere<br />

degradation and keep protective caps on the<br />

end of cell DNA indefinitely. 1 Were this to<br />

be accomplished, the cells would be able to<br />

divide an infinite number of times before they<br />

started to lose valuable genetic code, which<br />

would theoretically extend the life of the<br />

organism as a whole.<br />

In addition, studies into telomeres have<br />

revealed new ways of combating cancer.<br />

Although there are many subtypes of<br />

cancer, all variations of cancer involve the<br />

uncontrollable, rapid division of cells. Despite<br />

this rapid division, the telomeres of cancer<br />

cells do not shorten like those of a normal<br />

cell upon division, otherwise this rapid<br />

division would be impossible. Cancer cells<br />

are likely able to maintain their telomeres<br />

due to their higher levels of telomerase. 3 This<br />

knowledge allows scientists to use telomerase<br />

levels as an indicator of cancerous cells, and<br />

then proceed to target these cells. Vaccines<br />

that target telomerase production have<br />

the potential to be the newest weapon in<br />

combating cancer. 2 Cancerous cells continue<br />

to proliferate at an uncontrollable rate even<br />

when telomerase production is interrupted.<br />

However, without the telomerase to protect<br />

their telomeres from degradation, these cells<br />

eventually die.<br />

As the scientific community advances<br />

its ability to control telomeres, it comes<br />

closer to controlling the process of cellular<br />

reproduction, one of the many factors<br />

associated with human aging and cancerous<br />

cells. With knowledge in these areas<br />

continuing to develop, the possibility of<br />

completely eradicating cancer and slowing the<br />

aging process is becoming more and more<br />

realistic.<br />

WORKS CITED<br />

[1]Genetic Science Learning Center. “Are Telomeres the<br />

Key to Aging and Cancer.” Learn. Genetics. March 1,<br />

2016. Accessed October 5, 2016.<br />

[2]Shay, Jerry W., and Woodring E. Wright. “Telomerase<br />

Therapeutics for Cancer: Challenges and New ...” Nature<br />

Reviews Drug Discovery. July 2006. Accessed October<br />

16, 2016.<br />

[3]“The 2009 Nobel Prize in Physiology or Medicine -<br />

Press Release.” The 2009 Nobel Prize in Physiology or<br />

Medicine - Press Release. Accessed October 4, 2016.<br />

Images from Veernavya via Freepik<br />

DESIGN BY Albert Han<br />

EDITED BY Katrina Cherk<br />

CATALYST | 11

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