Washington, September 18 : University of Rochester biologists claim to have discovered a novel anti-cancer mechanism in small-bodied rodents with long lifespans.
Writing about their findings in the journal Aging Cell, the researchers said that the mechanism they had found appeared to be different from any anti-cancer mechanism employed by humans or other large mammals.
They believe that understanding this mechanism may help prevent cancer in humans because many human cancers originate from stem cells, and similar mechanisms may regulate stem cell division.
"We haven't come across this anticancer mechanism before because it doesn't exist in the two species most often used for cancer research: mice and humans. Mice are short-lived and humans are large-bodied. But this mechanism appears to exist only in small, long-lived animals," says Vera Gorbunova, assistant professor of Biology at the University of Rochester, a principal investigator of this study.
She believes that cells of the rodents her team has studied are hypersensitive to cues from the surrounding tissue.
According to her, the cells slow down cell division if they sense any inappropriate conditions for growth, a mechanism that can 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.
She says that her findings can be used to compare size and lifespan across several different-sized but closely related animals.
Her team has 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.
Scientists have long believed that an animal that lived as long as humans do needed to suppress telomerase activity to guard against cancer.
Since telomerase helps cells reproduce, and cancer is essentially runaway cellular reproduction, an animal living for 70 years has a lot of chances for its cells to mutate into cancer.
Given the relatively short life expectancy among mice, it was thought that the animal could afford the slim cancer risk to benefit from telomerase's ability to speed healing.
However, the latest study has revealed that it is the body mass that regulates the expression of telemerase, not life expectancy.
Simply having more cells increases the likelihood that one will become cancerous, and humans would likely develop cancer much more often and much earlier if telomerase was not suppressed.
Gorbunova and her colleagues also found that the common grey squirrel naked mole-rat, chipmunk, muskrat, and chinchilla expressed high levels of telomerase, which could increase their cancer risk over their long lifetimes.
However, such species had developed a mechanism to counteract the high telomerase activity, and remain cancer free for the duration of their lifespans, said the researcher.
"Squirrels know a cure for cancer. Short-lived small species display continuous rapid proliferation of their cells, but these long-lived rodents have somehow found a way to slow down that proliferation when they need to," says Gorbunova.
She thinks that squirrels and similar rodents have evolved a strict monitoring function within their cells that may be able to sense appropriate and inappropriate cell division, and slow or inhibit the division if necessary.
Her team is trying to isolate and understand this mechanism with the hope that it may be applicable to help human cells thwart the onset of tumour growth.