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Elephants rarely get cancer because their body is a rare ‘zombie gene’

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Rare ‘zombie’ gene that fights cancer found in elephants

A look at how a rare ‘zombie’ gene discovered in elephants fights cancer

Cancer is a friend to no one, but a “zombie gene,” known as LIF6, which still exists in elephants, may be useful in helping to end this deadly disease.

LIF6 is a gene that death is gone in virtually any other animal, except for the elephants, but researchers have shown that LIF6 is responsible for the control of cancer mutations in elephants, which are rarely get the disease.

In the study, published in Cell Reports, researchers Juan Manuel Vazquez, Michael Sulak, Sravanthi Chigurupati and Vincent J. Lynch turns out that elephants can be crucial for the understanding of Peto’s paradox, which states that “there is no correlation between body weight and cancer risk across species.”

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“Here, we show that elephants and their extinct relatives (proboscideans) can resolve Peto’s paradox, in part by refunctionalizing a leukemia inhibitory factor pseudogene (LIF6) with pro-apoptotic functions,” the researchers wrote in the study summary.

She continues: “These results suggest that refunctionalizing of a pro-apoptotic LIF pseudogene may be permissive (but not sufficient) for the evolution of large body sizes in proboscideans.”

“Genes in duplicate all the time,” said Dr. Lynch, assistant professor in human genetics at the University of Chicago and the study’s senior author, in an interview with the University of Chicago. “Sometimes they make mistakes, production of non-functional versions known as pseudogenes. We often refer to this dismissively as dead genes.”

Lynch and his colleagues were initially studying the p53 gene in elephants, but found that LIF6 (leukemia inhibitory factor 6) effectively have evolved to create a new “on” switch, bring him back from the dead.

“So, zombie,” Lynch told the University of Chicago. “This dead gene came back to life. When it is turned on by a damage of the DNA, it kills the cell, fast. This is good, because it behaves in response to genetic mistakes made when the DNA is restored. Getting rid of that cell can prevent a subsequent cancer.”

Elephants have 20 copies of the p53 gene in their genome, while human only have one. This gene is known as a tumor suppressor, according to an article in 2015 the Nature.

As soon as the LIF6 gene is activated by p53, it kills the affected cell fairly quickly, producing a protein that ultimately destroys the cell, the mitochondria, causing the cell to die.

When the LIF6 gene was blocked within the elephants, the sick cells eventually cancer.

Interestingly enough, when the LIF6 gene was introduced to animals that do not have activated, or lack of it, such as mice, she was also cancer-resistant.

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The potential impact

“Elephants get cancer much less than we would expect on the basis of their size, so we want to understand the genetic basis for this form of cancer resistance,” Dr. Lynch added in the comments obtained by the Daily Mail.

The impact of cancer-killing drugs could have on the population would be nothing less than amazing.

According to the National Cancer Institute, it is estimated that in 2018, will see approximately 1.74 million new cases of cancer in the united states and 609,640 people will die from the disease.

The NCI adds the most common forms of cancer (in descending order according to the estimated new cases), breast cancer, lung cancer and bronchus cancer, prostate cancer, colon and rectum cancer, while mentioning a number of others.

“From an evolutionary biology perspective, it is completely fascinating,” pediatric oncologist Joshua Schiffman told National Geographic.

Scientists now hope that drugs that mimic the effects of the LIF6 gene could lead to new forms of cancer treatments for humans in the not-too-distant future.

“Maybe we can find ways of developing drugs that mimic the behaviour of the elephant LIF6 or of getting cancer cells to turn on their existing zombie copies of the LIF gene,” Dr. Lynch said.

Follow Chris Ciaccia on Twitter @Chris_Ciaccia

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