More cells means more cell division, and as a loss of control in division regulation can lead to cancer. So one would expect larger animals to have a higher risk of developing cancer, right? Wrong. This month researchers from the University of Utah, led by Joshua Schiffman studied elephants in captivity, and estimated they were 20% less likely to die from cancer.
Schiffman and his colleagues explored these mechanisms of cancer resistance and provided evidence supporting the existence of this phenomenon – Peto’s Paradox. Blood samples revealed that African elephants inherit from each parent a minimum of 20 copies of a gene involved in signalling DNA damage in a cell – the p53 gene. The human Li-Fraumeni syndrome (LFS) arises when someone possesses a defective p53 gene and leads to a catastrophically high risk of cancer during a persons’ lifetime. When stress is detected, it is thought p53 halts cell division until repair is complete.
When Schiffman and his team exposed elephant and human LFS blood cells to radiation they predicted elephant cells would be better at repairing their DNA than human LFS cells. In fact the reverse was found – when elephant cells had damaged DNA they were twice as likely to die compared to human control cells, and LFS cells were much less likely. From an evolutionary perspective this makes sense – killing a cell kills the cancer.
If replicated, these findings could validate exploring the mechanisms of cancer suppression from an evolutionary perspective. Schiffman and colleagues intend to investigate the potential ways the p53 gene could be used in clinic treatment of cancer and its prevention, for example they have suggested technological advances such as using nanoparticles to deliver genes into damaged cells could be the next step on the long road to curing cancer.