Larger Animals and Cancer Rates
Larger animals have more cells in their bodies, and cancer occurs when one cell suffers the right combination of mutations to run amok, so why is it that animals such as whales do not have higher cancer rates? Here researchers propose a partial answer to that question:
Larger species do not have higher cancer rates than smaller species, an observation known as Peto's paradox, named after the eminent Oxford cancer epidemiologist Sir Richard Peto who first remarked on the phenomenon in the 1970s. "Cancer is caused by errors occurring in cells as they divide, so bigger animals with more cells ought to suffer more from cancer. Put simply, the blue whale should not exist."Now a study of the genomes of 38 mammal species, ranging in size from the mouse to the blue whale, has resulted in a partial explanation for the paradox - larger animals are just better at eliminating cancer-causing viruses from their DNA. A team of [scientists] analysed the genomes for DNA sequences of endogenous retroviruses (ERVs), which are viruses that are able to integrate their DNA within the DNA of the human chromosomes. The researchers found that there was an inverse relationship between the number of endogenous retroviruses - "relics" of viral infections over many millions of years of evolution - and the overall size of the species in question.
In other words, the bigger the animal, the fewer the number of viral relics found in its genome. The mouse for instance has 3,331 endogenous retroviruses, humans have 1,085 and whales have just 55 viral relics. This is seen as important for Peto's paradox on cancer rates because these retroviruses can jump around within the genome and in doing so trigger those kinds of cancer that are linked with viral infections, such as the T-cell leukaemia. Showing that larger species of animals have fewer ERVs in their genomes indicates that these kinds of viruses must be harmful, otherwise there would be no need to remove them. "Logically we think this is linked to the increased risk of ERV-based cancer-causing mutations and how mammals have evolved to combat this risk. So when we look at the pattern of ERV distribution across mammals it's like looking at the 'footprint' cancer has left on our evolution."
An interesting experiment would be for someone to use CRISPR to remove the DNA sequences of endogenous retroviruses from a strain of mice and see if this reduces their cancer rates versus controls. Germline engineering would probably be easier, but gene therapy in adults could be relevant to humans (and would be a target for companies such as Editas Medicine).