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Traditionally, cancer research and aging research focused on using mice or rats
Our philosophy here is that we can learn a lot more from looking at species that are long-lived and are cancer-resistant.
because there are specific mechanisms that contribute to long life, then mice may just not have those mechanisms.
Naked mole rats are very special.
They live really long, they live for 32 years.
We’ve never observed in them spontaneous cancer in these animals... And that was the main point of our research
We want to understand how this animal with a mouse’s size lives ten times longer and never gets cancer.
All mammals are pretty similar in genome composition.
So I think whatever we can learn from studying mice there are many things that we can apply to humans.
it seems like naked mole rats are even closer to humans than mice, which makes them even more valuable.
It looks like the naked mole rat has a two-tier mechanism to arrest the cell proliferation and in response to cell density.
First they were growing to a low-cell density, then it triggers some known tumor suppressors like P 16
when you isolate the primary cells from any other rodents, they’ll fill the plates to a completely confluent stage.
In the case of the naked mole rat, they still have a lot of space in between them, and they get the cell cycles arrested.
And this is a really powerful anti-cancer mechanism.
But in case of the blind mole rat, the cells are proliferating and are dividing only fifteen or twenty times in tissue culture.
And then, mysteriously as we observed the first time, it triggers as we call it: concerted cell death.
The whole population of cells dying in a matter of two days.
And that was really magic -- we couldn’t understand what was going on.
So we look after the target, what actually triggers the massive cell death in blind mole rat culture.
And what we discover is interferon beta, which is produced by the blind mole rat cells in response to hyperproliferation signals.
It means that the blind mole rats have a safety mechanism.
to eliminate the whole surrounding area of the cancerous cells and potentially probably killing the cancer.
So we have the same genes, but they’re just regulated differently.
They're not activated in the same way.
If in humans this mechanism is not being actively used, it means that we
can transfer it from mole rats to humans, so this is something we can benefit from.
Our goal is to identify mechanisms that can contribute to this diversity of lifespans
and then once we find them, we can use them hopefully to extend human lifespans.
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