University of Rochester researchers have discovered that small rodents with long lifespans, such as squirrels or chinchillas, can live decades without developing any form of cancer. Apparently, these rodents are using a previously unknown anti-cancer mechanism different from the ones used by humans or other large mammals. The lead researcher says that 'squirrels know a cure for cancer.' These long-lived rodents have apparently found a way to detect cancer development and to slow down cell division when it's needed to stop the cancer before it becomes dangerous. Will this self-monitoring anti-cancer mechanism ever be used by humans? Right now, it's still unknown, but read more...
As you can see above, "rodents present a wide variety of lifespans and sizes." (Credit: Vera Gorbunova, UR) Here is a link to a research page about Comparative Biology of Aging which contains a larger version of this picture. "Rodents are a phylogenetically related, yet their lifespans are extremely diverse ranging from 2-4 years in mice and rats to over 20 years in naked mole-rats, beavers, porcupines, and squirrels. [...] We are studying relation between DNA repair, genome stability and lifespan in short and long-lived rodents."
This research project has been led by Vera Gorbunova, assistant professor of biology at the University of Rochester. She worked with several colleagues in her lab. She also collaborated with scientists from the University of San Paulo and Vanderbilt University.
Here is how Gorbunova explains why this anti-cancer mechanism has not been discovered before. "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."
And here additional details about these findings. "Until Gorbunova's research, the prevailing wisdom has 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 colleagues showed that it was not life expectancy, but body mass that regulated the expression of telomerase. Simply having more cells increases the likelihood that one will become cancerous. We humans, as large animals, would likely develop cancer much more often and much earlier if we didn't suppress our telomerase."
This research work has been published in Aging Cell under the title "Distinct tumor suppressor mechanisms evolve in rodent species that differ in size and lifespan" as an 'Early View' article (September 2008).
Here is the beginning of the abstract. "Large, long-lived species experience more lifetime cell divisions and hence a greater risk of spontaneous tumor formation than smaller, short-lived species. Large, long-lived species are thus expected to evolve more elaborate tumor suppressor systems. In previous work, we showed that telomerase activity coevolves with body mass, but not lifespan, in rodents: telomerase activity is repressed in the somatic tissues of large rodent species but remains active in small ones. Without telomerase activity, the telomeres of replicating cells become progressively shorter until, at some critical length, cells stop dividing. Our findings therefore suggested that repression of telomerase activity mitigates the increased risk of cancer in larger bodied species but not necessarily longer-lived ones. These findings imply that other tumor suppressor mechanisms must mitigate increased cancer risk in long-lived species. Here, we examined the proliferation of fibroblasts from 15 rodent species with diverse body sizes and lifespans."
Sources: University of Rochester News, September 17, 2008; and various websites
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