Why do elephants have low cancer rates?

DO YOU KNOW Why do elephants have low cancer rates? Scientists have recently discovered a very new fact. According to scientists, elephants contain genes that protect elephants from cancer.

The research was conducted by Vincent Lynch of the University of Buffalo. And Juan Manuel Vazquez of the University of California. According to researchers, the risk of cancer also increases when the body size of organisms increases. But elephants are an exception. Researchers have concluded that elephants have cancer resistance.

According to researchers, tumor-suppressing genes are found in large numbers in elephants. Elephants, in particular, have genes for repairing DNA, reducing oxidative stress, developing cells, and handling the process of aging and death.

According to researcher Vazquez, the research on elephants has opened the door to the possibility of treating cancer with the help of this type of gene in the future. In addition to elephants, similar genes are also found in animals including Golden Moles, Elephant Shrubs, Rock Hirex, Mantis.

Why do elephants have low cancer rates?
Why do elephants have low cancer rates?

The body size of the elephant has become so big due to the tumor-resistant genes in the body. The slower metabolism of large animals such as elephants and whales may also play a role in their lower cancer rates. More-intense energy production leads to more cell division, and thus a higher risk of mutations. Just as some creatures are more adept at fending off tumors, others are particularly vulnerable.

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How do elephants prevent cancer?

Three years ago, oncology researchers discovered that elephants have 20 copies of p53, a gene that’s essential to cancer suppression. Humans, by contrast, have just one copy of p53. The researchers, which included a team at the University of Chicago, conclude that elephants are especially resistant to cancer because of p53. But they didn’t know the exact mechanism by which the tumor suppressor gene works.

Now the Chicago team has uncovered a key part of that process: a nonfunctioning, or “zombie” gene. The gene, called LIF6, is activated in elephants by p53, after which it kills cancer precursor cells. They believe that the discovery, which they described in the journal Cell Reports, could boost efforts to develop drugs for people that target p53.

Cells that are unable to repair DNA damage often go on to become cancerous. Elephants are estimated to have 100 times as many of these cancer precursor cells as people do. But less than 5% of captive elephants end up dying from the disease. To try to figure out why that is, the University of Chicago team has been studying elephant cells.

The scientists discovered that in elephants, LIF6 makes a protein that zooms to the damaged cells’ mitochondria, or energy center. And pokes holes in it, which causes cell death.

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Author Vincent Lynch Said

“When [LIF6] gets turned on by damaged DNA, it kills that cell, quickly,” said senior author Vincent Lynch, Ph.D., assistant professor of human genetics at the University of Chicago, in a press release from the university. “This is beneficial because it acts in response to genetic mistakes, errors made when the DNA is being repaired. Getting rid of that cell can prevent subsequent cancer.”

The team made the discovery by first inducing DNA damage in elephant cells and cells taken from smaller animals. The elephant cells died immediately, they observed. Then they tried blocking LIF6 protein expression, and the cells started to become cancerous. So they decided to try over-expressing LIF6 in cells from mice, which don’t normally have functional copies of the gene. All of the cancer precursor cells died.

Although p53 has been known as a tumor suppressor for quite some time. Efforts to translate that knowledge into drugs have been slow to materialize. Still, interest in p53 research remains high. Startup PMV Pharma raised $74 million from venture capitalists last year to develop a pipeline of p53-targeted cancer drugs. Its approach is to use small molecules to restore the function of the gene in cancers marked by p53 mutations.

Late last year, Stanford scientists announced they had found a p53 mutation that strengthens the ability of the gene to battle pancreatic cancer. The mutation regulates a cancer-promoting protein called Yap, they said. Their plan was to further study the mutation to determine if it’s active in other cancer types. 


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