Elephant genes hold clues for human cancer fight

Yet they don’t. The cancer mortality rate for elephants is less than 5% compared with 25% in people, the study said.

Since elephants have 100 times as many cells as people, they should be 100 times more likely to have a cell slip into a cancerous state and trigger the disease over their long life span of 50 to 70 years.

CHICAGO | Cancer is much less common in elephants than in humans, even though the big beasts’ bodies have many more cells.

Previous research has suggested that specific molecular mechanisms in elephants protect them against cancer, though Dr. Schiffman and colleagues note that such mechanisms are poorly understood.

Peto’s paradox is a name given to a mystery by scientists as to why elephants and other large mammals do not get cancer more often than smaller mammals.

Joshua Schiffman, an oncologist at the University of Utah School of Medicine in the U.S., who co-led the research, said: “By all logical reasoning, elephants should be developing a tremendous amount of cancer, and in fact, should be extinct by now due to such a high risk for cancer”.

To find out, he teamed up with Maley, an elephant keeper at Utah’s Hogle Zoo in Salt Lake City and the chief veterinarian for the Ringling Bros and Barnum & Bailey Circus. They said that African elephants have 20 copies of a gene, called TP53, which has the ability to create protein that suppresses tumors.

“Nature has already figured out how to prevent cancer”. Schiffman’s patients include children with incomplete p53 genes because of a condition called Li-Fraumeni syndrome, which greatly increases their chances of developing cancer. To see whether this could be the case, the researchers collected white blood cells from elephants and humans and exposed the cells to radiation that caused their DNA to break.

Applying the translational research around cancer – the findings from the basic science enhancing human health and well-being by improving medical and nursing practices and creating meaningful health outcomes – could pave the way for an entirely new frontier of cancer research and treatment, from the laboratory bench to the bedside. The gene immediately works on the spot of DNA damage and stops the cells from replicating thus repairing the DNA.

Trevor Graham, who studies tumour biology at the Barts Cancer Institute at Queen Mary University of London, said the findings are exciting. Cancer involves uncontrolled cell growth. “The implication for humans is that reinforcing the protection offered by [TP53] would be enough to prevent our own cells from becoming cancerous”. If p53 develops a fault it can leave people at the mercy of cancer.

Another thought is to insert more TP53 genes into precancerous cells. While studies in humans are at least several years away, “we certainly think we’ve found something very intriguing”, Schiffman said. “We want to learn how to take advantage of that”.