Potential Cancer Resistance
How it works
Cancer proliferation is characterized by uncontrolled and unregulated cell growth resulting in tumors. In theory, as the size of organism increases there are more cells developing and dividing meaning that this is an increased probability of cancer development. Although, this response is theorized this is not what actually occurs, but why this trend is observed remains poorly understood. The present study aimed to understand these mechanisms of cancer suppression in large, vertebrate mammals in hopes of gaining insight to human cancer physiology.
Necropsy data on a variety of vertebrate animal deaths was collected in order to determine if cancer rates varied due to body size and lifespan. Researchers compared blood samples of African and Asian elephants to humans without a significant family history of cancer, which were used as the control. Elephant genomes were then analyzed the TP53 gene and other retrogenes were evaluated to determine their expression and number in elephants. After DNA damage was done to both human and elephant samples, the repair rates and cell cycle arrest were measured and compared. From the microscopy data, the investigators determined that rates of cancer did not increase with increasing body mass and lifespan.
The elephant peripheral blood lymphocytes had greater rates of apoptosis than that of the human control samples, but this could not be linked to DNA damage. Expression of the TP53 gene did not increase in elephants, but expression did increase in human PBLs following DNA damage. Researchers concluded that the many copies of the TP53 genes present in the elephant genome and the increased instances of p53-mediated apoptosis, provide evidence supporting cancer suppression mechanisms in elephants. There is also evidence that supports the conclusion that less DNA damage is tolerated in elephant cells before apoptosis is triggered, in comparison to humans.