Elephants: Large, Long-Living and Less Prone to Cancer(nytimes.com)
nytimes.com
Elephants: Large, Long-Living and Less Prone to Cancer
http://www.nytimes.com/2015/10/13/science/why-elephants-get-less-cancer.html
13 comments
If larger animals had better cancer fighting weapons, then the largest animals ever on the planet, the blue whale, being 15-25x larger, would have that much better cancer fighting weapons. I wonder what those would be.
They do. Evolution.
They needed to evolve to reach a certain age ( -> once they cant reproduce anymore) without dying to cancer. https://www.youtube.com/watch?v=fMMPKJFYzdY for a more in depth explaination
They needed to evolve to reach a certain age ( -> once they cant reproduce anymore) without dying to cancer. https://www.youtube.com/watch?v=fMMPKJFYzdY for a more in depth explaination
At some point you're so big cancer will mutate to death before it can kill you.
At that size, the cancer itself can get cancer.
Experiments in which mice get extra amounts of p53 have shown that the molecule has a downside: It can accelerate aging.
This bothers me. What exactly is the relationship between cancer and aging?
This bothers me. What exactly is the relationship between cancer and aging?
There is a theory that has substantial evidence that "senescence" the technical term for aging is a defense against cancers. Here is a long article about how cancer and senescence are related.[0]
[0]http://www.nature.com/nature/journal/v448/n7155/full/nature0...
[0]http://www.nature.com/nature/journal/v448/n7155/full/nature0...
Correlation, but what could the causation possibly be? Cancers and senescence occur late in life, past the reproductive age. Doesn't that mean the correlation cannot be selective?
The article goes into more depth but it's more than just the correlation that aging and cancer both occur with age.
One neat thing the article brings up has to do with the p53 protein. People who have only one functional copy of this enzyme have Li–Fraumeni syndrome. Basically they get lots of cancer. On the other hand mice who over express the p53 protein don't get any cancer but age more quickly than other mice.
There exists a similar dimension for telomeres. If you have to few you are at higher risk for developing senescent related diseases. If you have too many you're prone to cancer.
Basically a senescent cell has decided not to divide anymore because it has determined it would be dangerous to do so. So many of the enzymes/chemicals/genes that push these cells to continue to divide cure senescence related illnesses but lead to higher risk of cancer.
One neat thing the article brings up has to do with the p53 protein. People who have only one functional copy of this enzyme have Li–Fraumeni syndrome. Basically they get lots of cancer. On the other hand mice who over express the p53 protein don't get any cancer but age more quickly than other mice.
There exists a similar dimension for telomeres. If you have to few you are at higher risk for developing senescent related diseases. If you have too many you're prone to cancer.
Basically a senescent cell has decided not to divide anymore because it has determined it would be dangerous to do so. So many of the enzymes/chemicals/genes that push these cells to continue to divide cure senescence related illnesses but lead to higher risk of cancer.
I'm no medical researcher, but I could make a guess. The article said that in elephants cells commit suicide when damaged.
It's well known that our cells have a maximum number of times they may divide. As they divide their telomeres become shorter. Once these telomeres reach their ends, the cells cannot further divide.
And so something that quickens the pace of cell destruction (via the p53 mechanism for spontaneous cell suicide), would then quicken the aging process.
Anyhow, I'm impressed by this research. It really shows Out of the box, back to basics sort of thinking. People cannot hope to alter the software of natural processes. The best we can hope for is copy pasting solutions when we find them.
It's well known that our cells have a maximum number of times they may divide. As they divide their telomeres become shorter. Once these telomeres reach their ends, the cells cannot further divide.
And so something that quickens the pace of cell destruction (via the p53 mechanism for spontaneous cell suicide), would then quicken the aging process.
Anyhow, I'm impressed by this research. It really shows Out of the box, back to basics sort of thinking. People cannot hope to alter the software of natural processes. The best we can hope for is copy pasting solutions when we find them.
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I wonder, exactly how might a cell "commit suicide"?
The medical term is "Apoptosis" and the Wikipedia article is a good intro to this very complex topic [1]
[1] https://en.wikipedia.org/wiki/Apoptosis
[1] https://en.wikipedia.org/wiki/Apoptosis
“All in all, it’s interesting, but the mechanism needs to be properly investigated,”
This is the type of academic bullsh@t that needs to stop. Of f@cking course more research needs to be done but let these people have their moment for advancing the field.
Life is literally too short to ruin it in this way.
This is the type of academic bullsh@t that needs to stop. Of f@cking course more research needs to be done but let these people have their moment for advancing the field.
Life is literally too short to ruin it in this way.