Scientists in the United States believe they have discovered a previously unknown anti-cancer mechanism in some rodents.
Biologists at the University of Rochester have found that small-bodied rodents with long lifespans have evolved a previously unknown anti-cancer mechanism that appears to be different from any anti-cancer mechanisms employed by humans or other large mammals.
They believe understanding how this mechanism works may help prevent cancer in humans because many human cancers originate from stem cells and similar mechanisms may regulate stem cell division.
The leading principal investigator of the study, assistant professor of biology Vera Gorbunova, says this anti-cancer mechanism has not been seen before because it doesn't exist in the two species most often used for cancer research - mice and humans.
Professor Gorbunova says mice are short-lived and humans are large-bodied and this mechanism appears to only exist in small, long-living animals.
Professor Gorbunova believes that the cells of long-living, small-bodied rodents are hypersensitive to cues from the surrounding tissue and if the cells sense that conditions are inappropriate for growth, they slow down cell division - this would arrest tumour growth and prevent metastases.
Gorbunova's team has worked at length investigating the links between body size and lifespan in rodents because rodents range in size from tiny field mice to the human-sized capybara of Brazil.
The researchers use them to compare size and lifespan across several different-sized but closely related animals and in the process discovered that telomerase, an enzyme that can lengthen the lives of cells, but can also increase the rate of cancer, is highly active in small rodents, but not in large ones.
Until this research it was assumed that an animal that lived as long as we humans do, needed to suppress telomerase activity to guard against cancer.
Telomerase helps cells reproduce, and cancer is essentially runaway cellular reproduction, so an animal living for 70 years has a lot of chances for its cells to mutate into cancer.
A mouse's life expectancy is shortened by other factors in nature, such as predation, so it was thought the mouse could afford the slim cancer risk to benefit from telomerase's ability to speed healing.
But Gorbunova and her colleagues have found that it was not life expectancy, but body mass that regulated the expression of telomerase and simply having more cells increases the likelihood that one will become cancerous.
Gorbunova says humans, being large animals, would likely develop cancer much more often and much earlier if the body did not suppress telomerase.