Interest in understanding the human genome is higher than ever, as is the desire to edit it, especially after realizing that some animals don’t have as many problems with cancer.

The advent of Crispr-CAS9 gene editing came after decades of attempts to gain insight into how human DNA is built and functions. Similarly, researchers have been searching for ways to fight debilitating diseases such as AIDS and various cancers.

Could a zombie gene in elephants and human “junk” DNA help cure cancer?

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image of elephants for article Why we Should Look to Junk DNA to Help Cure Cancer
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Problem: Peto’s Paradox

In a move divisive from most accepted theories of evolution, elephants have a gene that acts a bit odd. Due to increased sensitivity to DNA damage, the large, tusked creatures are less prone to cancer. Any anomalies are detected early and dealt with swiftly before the disease can spread.

image of Richard Peto for Peto's Paradox in article Why we Should Look to Junk DNA to Help Cure Cancer
Richard Peto | PLOS Blogs

Conversely to what you might think, larger mammals (with more cells) have fewer instances of cancer. As a result of the discovery of cancer epidemiologist Richard Peto, we understand this phenomena as “Peto’s Paradox”. It has to do with the amount of time an organism is exposed to a malicious mutation.

Due to the nature of how DNA replicates (copying itself billions of times), body mass should affect the frequency of cancer. But therein lies the paradox.

As current research supports, larger mammals experience fewer instances of cancer. With elephants, in particular, they use a resurrected pseudogene (hence the “zombie gene” epithet).

Solution: Time, Genes, Body Mass, and Je Ne Sais Quois

The solution to the paradox for humans could be in observing the evolution of other animals. Specifically, scientists are looking at facilitating extra copies of the TP53 gene. Elephants evolved over long periods of time to become more sensitive to DNA damage. This led to a decrease in the occurrence of cancer in the species. But blue whales, also a large organism, did not develop their evolutionary protection in the same way.

By understanding how large organisms develop cancer protections, humans might be able to prevent instances of cancer moving forward. However, solving Peto’s Paradox is not the only weapon in our biological research arsenal.

image of microscope for biological research and DNA study in article Why we Should Look to Junk DNA to Help Cure Cancer
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Genetic Material Readily Available for Improved Research

Nearly 500,000 volunteers offered 3 million samples of their genetic material to this biobank for use in future medical studies. The NSW Government plans to have this health initiative decrease the time it takes to make medical breakthroughs. By providing easy-to-access, cataloged samples, researchers can focus more.

Having access to all kinds of genetic material means that human “junk” DNA is also available. Studying never before considered sequences of DNA could produce nothing. Or, it could produce significant findings.

After all, in 2016, the Universities of Bath and Cambridge both linked junk DNA to the curtailing of breast cancer. As a result, pseudogenes or genes with seemingly no purpose could become integral in future cures.

A Hidden Clue & Another Step Closer to Curing Cancer

Consider also genome sections like HSAT-II which is usually dormant in healthy cells. Due to its non-functioning state, researchers have long ignored it. However, Jeanne Lawrence, PhD, and her team found that, in cancer cells, HSAT-II wasn’t dormant.

image of DNA as puzzle for article Why we Should Look to Junk DNA to Help Cure Cancer
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Fellow researcher in the HSAT-II project, Lisa Hall-Anderson, PhD, told Medical Express this:

“This repetitive ‘junk’ in our genome is a giant blank spot where the sequences haven’t been mapped. Researchers rarely look at them. This junk, though, may also be what plays a role in control of our genes.”

What else do you think the human genome could be hiding amid mutations, cell division, and “junk” DNA?

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